(based on Prof. James Diaz lecture slides)
A: Two
Q: _ Cells Are Support Cells
A: Glial
Q: _ Cells Are the Main Signaling Units of the Nervous System
A: Nerve
Q: _ Is organized in the same way in all nerve cells
A: Signaling
Q: The Input Component Produces _ Local Signals
A: Graded
Q: The _ Component Makes the Decision to Generate an Action Potential
A: Trigger
Q: The _ Component propogates in all-or-none action potential
A: Conductile
Q: The _ Component Releases Neurotransmitter
A: Ouput
Q: The Central Nervous Sytem Has Seven Major Divisions
A: Spinal Cord, Medulla, Pons, Midbrain, Cerebeullum, Diencephalon, Cerebral Hemispheres
Q: Each _ System Involves Several Brain Regions That Carry Out Diffrent Types of Information Processing
A: Functional
Q: Identifiable Pathways Link the _ of a Functional System
A: Components
Q: Each Part of the Brain Projects in an Orderely Fashion Onto the Next, Therby Creating _ Maps
A: Topographical
Q: Functional Systems are _ Orgnised
A: Hierarchically
Q: Functional Systems on One Side of the Brain _ the other side of the Body
A: Control
Q: _ Principles Govern the Organisation of the Major Functional Systems
A: Components
A: 1) Action Potential 2) Synaptic Potential 3) Generator Potential
Q: Neuronal electical signals represent variations of the:
A: electrical potential diffrence across the neuronal membrane
Q: Neuronal electrical signals are disturbances of the:
A: resting in a neuron
Q: The membrane of neurons have an electrical charge on them due to the:
A: peculiar distribution of charged particles on either side
Q: Typically, the inside of a neuron at rest (not actively signaling) is _ relative to the outside
A: negative
Q: The difference in electrical charge (the separation of charge) across the neuronal membrane is called the:
A: membrane potential (VlowerM)
Q: The mebrane potential (VlowerM) of a neuron that is not conducting or signaling is called the:
A: "resting membrane potential" or VlowerR
Q: Neuronal signaling involves in one way or another, changes in the:
A: Resting membrane potential (VlowerR)
Q: An increase in the potential or in other words, making the inside more negative is called
A: hyperpolarization
Q: A decrease in the potential, or making the inside of the neuron more positive is called
A: depolarization
Q: Many substance will split into parts each with opposing electrical charge when the substance is dissolved in water. These substances are called _ and the charged particles are called _.
A: electrolytes ions
Q: Those ions with positive charge are _ and those with negative charge are called
A: cations, anions (ex salt Na+ Cl-)
Q: The peculiar distribution of ions on either side othe neuronal membrane AND the forces involved with these gradients are the keys to
A: neuronal transmission
Q: At rest, there are four ions of interest: One critical factor in this distribution is the membrane itself, more specifically the _ in the membrane
A: sodium- Na+ potassium - K+ chloride - Cl- large proteing molecules inside the neuron [pores or channels]
Q: The neuronal membrane is made up of a double lipid layer, studded with proteins. The inner portion is highly _
A: hydrophobic (water repellent).
Q: Two principle parts of the membrane: 1. polar head (containing phosphate) which is water - 2.two fatty acid tails which are water -
A: soluble insoluble
Q: The proteins of the membrane can be etiher: - which means they are attached to the membrane; or - which are not attached
A: intrinsic; extrinsic
Q: Ions will attract water molecules. The - are electostatically bound water molecules to ions (cation attract the - part, anions atract the - part)
A: water of hydration, oxygen, hydrogen
Q: Since ion will be carrying water of hydration they will not be able to go through the _ membrane and therefore need a specialized channel for passage
A: neuronal
Q: Ion channels are - proteing complexes that span the neuronal membrane. There are two general types of channels: - and - channels
A: alpha-helical, gated , non-gated
Q: There are three importan propreties of gated channels: 1. They [] ions- they provide a hole through which ions can cross the membrane. 2 They [] for specific ions 3. they open and close depending to a) [] stimuli (namely VM) b) [] stimuli (as in skin depression) c) to [] stimuli (the presence of certain molecules)
A: conduct, select, electrical, mechanical, chemical
Q: - are NOT open all the time but rather flick open and closed randomly and continously and it is not clear what riggers these openings and closings
A: Non-gated passive channels
Q: Non-gated, passive, channels also: 1.- they provide a hole thrhough which ions can cross the membrane 2.-
A: 1.conduct ions 2. select for specific ions
Q: - channels are found through the entire neuronal membrane, unlike the specific distribuions of the - channels
A: non-gated passive, "gated"
Q: Ion size varies, Na+ is - than K+; however the "hydration shell" is inveresely proportaional to size. So that Na+ has a - shell than does K+
A: smaller ; larger
Q: There appears to be a - in these non-gated/passive channels. It is located somewhere in the lumen of the channel and it forms a weak and brief bond to the ion that is passing through.
A: "selectivity filter"
Q: The flow of ions will - which is consistent with the model of a brief binding at some recognition site in the lumen of the channel
A: saturate
Q: If one considers that a ion channel is typically made up of at least - alpha helical structures one can see that there may be ample opportunity for an ion to "stick"/bind on the way through a channel.
A: four
Q: In general, channels select the types of ions at pass: 1) on the basis of ionic - (cation vs. anion) 2) Some cation channels are non selective for the various - 3) some cation channels are more selective for - and - vs - 4. all anion channels are slective for -
A: 1. charge 2. cations 3. Na+ and K+ vs. Ca++ 4. Cl-
Q: The kinetics of ion flow through a channel depends on: 1. - of the ion 2. - characteristics 3. - driving force a) electostatic force
A: 1. size 2. channel 3.electochemical
Q: The actual ion flow through a channel will also depend on the [] of the membrane. []is the number of open- available- holes.
A: permeability permeability
Q: What if the membrane was totally permeable to only K+ ? Consider 1. - is higher inside (400) that outside (20) and that driving K+ OUT of the neuron 2. electostatic force: the inside of the neuron is NEGATIVE relative to the outside, so the electrostatic force is keeping K+ INSIDE the neuron
A: concentration gradient force;
Q: Initially, [] ions will stream out of the neuron. Each [] ion that leaves makes the inside even more negative. When enough [] ions have left, the inside of the neuron will be so negative that it will preven any more [] ions from leaving. The value of VlowerM when this balance occurs is called the [](Elowerx). This relationship is descrived by the []. The Equilibrum Potenintial for [] is Elower[]= []
A: K+, Equillibrum Potential, Nernst Equation, K+, -75mv
Q: The [] is the value of VM when concentration gradient forces and electostati forces are at balance for (or when there is no net flow of) a particular ion.
A: Euillibrum Potenintial
Q: What about the Equillibrum Potential Na+. 1. Concentration gradient force inside Na+ (50) is lower than outside (440), so the concentration gradient force is driving Na+ INTO the neruon 2.
A: deplolarizing
Q: The Action Potential is 1) a large depolarizing wave that 2) [] propagates itself down the axon 3) without losing amplitude.
A: actively
Q: The Action Potential is 1) a large depolarizing wave that 2) [] propagates itself down the axon 3) without losing []
A: amplitude
Q: Beginning with the axon hillock and for the length of the axon there is a particular class of channel- the Potential [] Channel
A: Sensitive
Q: Potential Sensitive Channels open and close in response to the value of []
A: VlowerM
Q: Along the axon, there are two kinds of these channels: 1)potential sensitive Na+ channels 2) potential sensitive K+ channels Both of these channels open to []
A: depolarization
Q: The depolarization wave of the action potential is due to Na+ []
A: influx
Q: The hyperpolarization wave of the action potential is due to K+ []
A: ouflux
Q: The "voltage clamp" performs three important functions: 1) [] 2) changes VlowerM to any determined value 3) adds current to either side of the membrane to maintain this VlowerM
A: 1) measure the VlowerM
Q: The "[]" breaks the dynamic feed forward process of the potential sensitive channels of the axon
A: voltage clamp
Q: A [] depolarization leads to a small and constant outward current, due to the change in driving force. The outward current is K+ and through the passive, non-gated channels.
A: SMALL
Q: After a [] depolarisation 1) the large capacitive membrane current 2. the "leakage" current due to current through the passive non-gated channels 3. the bi-phasic current flow, that is inward and outward of the neuron.
A: LARGE
Q: The defenition for threshhold that book offers could also serve as a functional definition for the action potential: Threshhold, VlowerT is that value of VlowerM when the net [] current changes from outward to inward.
A: ionic
Q: The substances Tetrodotoxin (TTX) and Tetraethylammonium (TEA) help to determine the individual characteristics of the potential sensitive channels of the []
A: axon
Q: [] (TTX) binds to and clogs up to Na+ potential sensitive channels only (NOT the Na+ passibe channels)
A: tetrodotoxin
Q: Tetraethylammonium (TEA) binds to and clogs up [] potential sensitive channels only (NOT the [] passive channels)
A: K+
Q: An axon bathed in [] would only have K+ potential sensitive channels functional
A: TTX
Q: An axon bathed in TEA would only have [] potential sensitive channels functional
A: Na+
Q: Similarities between potential sensitive channels: 1) both open to depolarisation 2) both have a [] (population) response the greater the depolarization
A: greater
Q: Dissimilarities between potential sensitive channels: 1) Na+ channels open [] rapidly than K+ channels open 2) If the depolarization persists, Na+ channels close, K+ do not 3) Na+ channels are faster to close (or K+ channels are slower)
A: more
Q: Dissimilarities between potential sensitive channels: 1) Na+ channels open more rapidly than K+ channels open 2) If the depolarization persists, Na+ channels [], K+ do not 3) Na+ channels are faster to close (or K+ channels are slower)
A: close
Q: Dissimilarities between potential sensitive channels: 1) Na+ channels open more rapidly than K+ channels open 2) If the depolarization persists, Na+ channels close, K+ do not 3) Na+ channels are faster to [] (or K+ channels are slower)
A: close
Q: The fact that a greater depolarization caused a greater conductance suggests that individual potential sensitive channels have different "thresholds" to [].
A: open
Q: Then one can consider [] sensitive channels as a "population" with a bell curve as to thier individual threshold to open.
A: potential
Q: The potential sensetive Na+ channels are [] to close than the K+ channels.
A: faster
Q: Na+ channels exist in one of three states: 1) closed - ready for opening 2) open 3) closed - []
A: refractory
Q: There is a brief period that follow an action potential in which is "refractory" that is cannont fire again. This is due to the "closed" state of the [] channels.
A: Na+
Q: There are two phases of periods of refractoriness: [] refractory- immediately following an action potential during which the neuron cannot be fired because the Na+ channels are all locked closed
A: absolute
Q: There are two phases of periods of refractoriness: [] refractory - right after the absolute refractory period, when an action potential can be fired only if the stimulus is stronger than usual. This may be due to the fact that the Na+ channels that become ready have different thresholds.
A: relative
Q: After period of time at VlowerR, only a portion of the Na+ channels are ready for opening. It would take a relatively large [] to open all of these newly available channels.
A: depolarization
Q: It takes some time at [] to cause the Na+ channels to be "ready" again 2. that time is different for the individual Na+ channels.
A: VlowerR
Q: There is no "in-between" stage for potential [] channels. These channels are either open or closed, but NOT half-way.
A: sensitive
Q: The characteristics of the Na+ and K+ potential sensitive channels as well as the concept of VlowerT are illustrated in the phenomenon of "[]"
A: accommodation
Q: Basically, "accomodation" is when a [] depolarization raises the VlowerM well passed a normally observed threshold before the neuron will generate an action potential
A: SLOW
Q: Under normal condition [] will cause an action potential
A: depolarization
Q: If the dipolarization is [] enough the VlowerM will depolarize well beyong its normal levels
A: slow
Q: "Accommodation" (which does not happen in nature) is due to the [] of K+ channels keeping with the slow depolarization of the Na+ channels. Since the depolarisation is slow, not enough Na+ channels open at any one point in time for an action potential to occur.
A: hyperpolarization
Q: The direction of the action potential, from the axon hillock towards the axon terminal is assured by: 1) the axon hillock having the lowest threshold to fire than any other section of the axon 2) the refractory period of the Na+ channels
A: lowest
Q: The direction of the action potential, from the axon hillock towards the axon terminal is assured by: 1) the axon hillock having the [] threshold to fire than any other section of the axon 2) the refractory period of the [] channels
A: Na+
Q: The action potential is usually followed by a brief period of hyperpolarization called the "After Potential". This is due to the slowness of the potential sensitive [] channels to close after activation
A: K+
Q: In addition to Na+ and K+, most neurons also have potential sensitive (voltage gated) Ca++ channels that open to depolarization; and potential sensitive (voltage gated) []
A: Cl-
Q: In addition to Na+ and K+, most neurons also have potential sensitive (voltage gated) [] channels that open to depolarization; and potential sensitive (voltage gated) Cl-
A: Ca++
Q: There are 4 types of [] potential sensetive/voltage gated channels
A: K+
Q: There are 2 types of [] voltage gated channels
A: Na+
Q: There are [] types of Ca++ voltage gated channels
A: 5
Q: The four types of K+ sensetive/voltage gated channels are: 1) slowly activated (delayed rectifier) 2. [] activated K+ channel which opens to depolarization by its voltage sensitivity depends on intracellular []
A: Ca++
Q: The four types of K+ sensetive/voltage gated channels are: 3) [] fast, transient activated by depolarisation (which comes in different flavors);
A: A-type
Q: The four types of K+ sensetive/voltage gated channels are: 4) [] Which is activated by depolarization but is inactivated by acetylcholine (ACh)
A: M-type
Q: Intraneuronal [] is a common modulator in most neurons. At rest, [] concentrations ae extremely low, much lower than intracellular Na+. Many intracellular mechanisms exploit this.
A: Ca++
Q: There is a Ca++ "pump" or buffering system in neurons that is very []. The Ca++ that comes in after one action potential can exceed its capacities and Ca++ begins to accumulate.
A: slow
Q: A series of action potentials (a train of voley) will increase intracellular Ca++ which will increase the probability of opening Ca++ activated [] channels which will be a hyperpolarizing effect.
A: K+
Q: Some Ca++ channels are themselves sensetive to intraneuronal Ca++, which will bing to the internal surface of these channels and eventaully will [] them.
A: close
Q: So Ca++ influx has 2 general effects: 1) contributes directly to [] of the action potential; and 2)contributes to hyperpolarization of the neuron
A: depolarization
Q: So Ca++ influx has 2 general effects: 1) contributes directly to depolarisation of the action potential; and 2)contributes to [] of the neuron
A: hyperpolarization
Q: The hyperpolarization of the neuron is due to two factors: 1) Ca++ will activate K+ channels causing K+ effluz; 2) Ca++ will [] its own influx by blocking its channels
A: decrease
Q: How a neuron respnds to [] is determined by the proportion of different type of petential sensitive/voltage gated channels in the neuron's axon hillock.
A: input
Q: Some neurons will respnd to constant excitatory input with: 1) a decelerating train of action potentials 2) an accelerating train of action potentials 3) a [] train of action potentials
A: constant
Q: In some cases, [] changes in PSP's will increase the firing rate, whereas in other neurons only large changes in PSP's will increase neuronal firing rates
A: small
Q: [] can lead to 1) a decrease in responsiveness to excitation; OR 2) an increase in responsiveness to excitation (due to the inactivation of Ca++ channels or the actvation of K+ channels)
A: Hyperpolarization
Q: Thus even in the generation of an action potential, there is flexibility in the process. This is the nature of [] "plasticity"- being able to vary the outcome of processing information
A: CNS
Q: If the synapse if bathing in TTX (therby shutting down potential sensetive [] channels), the PSP is lost as soon as the presynaptic side fails to depolarize
A: Na+
Q: If one can ARTIFICIALLY depolarize the preshynaptic side, then regardless of TTX and/or TEA, a PSP will be produced if the presynaptic side depolarizes greater than [] mV
A: 40
Q: In the case of TTX and TEA, the PSP stays on much longer than with only TTX. This is because the [] prevents the hyperpolarization of the presynaptic side.
A: TEA
Q: The potential sensetive K+ and Na+ channels are not mediating the Action Potential-induced PSP. [] movement AT THE AXON TERMINAL is the critical factor in the generator of a PSP
A: Ca++
Q: Decreasing extra-cellular [] concentrations will ultimately block the PSP; and Increasing extra-cellular [] concentration will increase the PSP. the more [] flows in the greater the PSP
A: Ca++
Q: There is a certain type of potential sensitive channel on the axon and specifically populates only axon terminal. These are a type of [] potential sensitive channels.
A: Ca++
Q: The are several types of potential sensitive [] channels: 1) the L type 2)the P/Q type 3) the N type 4) the R type 5) the T type
A: Ca++
Q: The L, P/Q. N and R types require relatively strong deplarization to open; whereas the [] type opens to smaller depolarizations
A: T
Q: The P/Q, N and R types are fast opening and the [] type is slower
A: L
Q: Of these types of potential sensitive Ca++ channels: 1) the L type that are slow to [] and 2) The N type that are fast to []
A: deactivate
Q: Therefor the faster types especially the N type are associated with exocytosis, and the [] type is not even localized in the area where transmitters are realeased. The [] type may be involved with neuropeptide release and vesicle mobilization.
A: L
Q: Just how Ca++ influz into the axon terminal mediates the PSP was discovered by [] with his discovery of the "miniature end plate potential"
A: Katz
Q: The synapse between a neuron and skeletal muscle in a distinctive synapse. The post synaptic surface is called the "end plate" and the [] is called the "end plate potential".
A: PSP
Q: "minature end plate potentials" are very small end plate potentials of about .5mV that occur randomly in the absence of an action potential. [] of the pre-synaptic side will increase the occurence of mini-end plate
A: depolarization
Q: The axon terminal has specialized organells called "synaptic vesicles" or just "vesicles" that store neurotransmitter molecules. The minature end plate potential appears to be the result of one vesicle dumping its content into the []
A: synapse
Q: A single [] channel can produce a .3uV PSP. A minature end plate potential of .5mV is the result of approxiamtely 2000 [] channels opening
A: POSTsynaptic
Q: A single vesicle holds approximately 5000 molecules of acetylcholine (ACh). It takes [] molecules of ACh to open a post-synaptic receptor
A: two
Q: The del Casillo/Katz hypothesis: 1) under normal conditions, the end plate potential of about [] mV is due to about 150 vesicles dumping into the synapse 2) variation in end plate potentials are the result of varying amounts of vesicles dumping
A: 70
Q: An essential feature of the [] terminal is the accumulation of vesicles in certain areas of the terminal. There is a presynaptic membrane thickening on the inner surface of the membrane called the "dense bar"
A: axon
Q: Dense bars are located directly opposite [] receptors sites AND synaptic vesiclles collect in rows along the top sides of the dense bars.
A: POSTsynaptic
Q: The dense bars and the congregation of vesicles together make up what is called the "active zone". The active zone is essentially where [] release occurs.
A: neurotransmitter
Q: The process wherebt synaptic vesicles in an axon terminal release their neurotransmitter moleculees into the synapse is called "[]". There is a pore on the vesicle and one that matches it on the axon terminal membrane.
A: exocytosis
Q: There are particles along the dense bars which are probably Ca++ channels of the [] type (type N) which appear to open upon depolarization
A: fast
Q: If vesicles keep "melting" or fusing into the membrane, the postsynaptic surface would swell. But vesicles are recaptured in a recycling process called []
A: endocytosis
Q: The actual mechanisms of exocytosis relies on a variety of proteins in the vesicles itself. These proteins are involved with four basic elements of exocytosis: 1) restraining the vesicles in the area above the active zone 2)herding the available vesicles to the active zone 3)doccking the vesicles 4) mediating the exocytosis 5) []
A: endocytosis
Q: [] keeps vesicles attached to filaments
A: synapsins
Q: Ca++ channels, of the [] type (type L) that are not in the active zone, appear to mediate the mobilization of these vesicles by causing the phosphorylation.
A: slow
Q: [] proteins will target and get the vesicles to the active zones
A: Rab
Q: Hydrolysis of the Rab GTP may serve to prevent vesicels from leaving the [] zone.
A: active
Q: During [] the Rab proteins are released
A: exocytosis
Q: There are two proteins involved in the [] : synaptobrevin and synaptogamin in the vesicle; and syntaxin and SNAP-25 on the membrane 9and Neurexin)
A: docking
Q: Dosking: First the Synaptobrevin in the vesicle which bings to the Syntaxin and [] on the membrane
A: SNAP-25
Q: Synaptogamin which also binds ot Syntaxin: this VAMP has a portion that binds to phosopholipids n [] dependent manner
A: calcium
Q: Synaptogmin may also play a role in []. It serves as a receptor for the clathrin adaptor protein which will coat the collapsed vesicle and help it get pinched off and returned to the cytoplasm
A: endocytosis
Q: Synaptic Plasticity is the process whereby neurotransmission can change its effectiveness - or how the resulting PSP can vary. It is mediated by altering the amount of [] coming into the presynaptic terminal.
A: Ca++
Q: There are two types of Synaptic Plasticity: 1. one governed by [] factors 2. and one governed by Extrinsic factors
A: Intrinsic
Q: For both of these types, remember that Ca++ enters the presynpatic terminal via potential sensetive channels, and that [] opens these potential sensitive Ca++ channels
A: depolarization
Q: Thus,[] at the terminal determines the amount of Ca++ that enters and thus controls the number of vesicles that are released into the synapse
A: VlowerM- the membrane potential-
Q: At VlowerR there are some Ca++ channels that are open, so that at VlowerR there is some Ca++ coming into the terminal Hyperpolarization will decrease the amount of this steady stream of Ca++ [].
A: influx
Q: The high frequency firing of a neuron (around 500-1000/sec) is called [] or tetanic simulation
A: tetanus
Q: The increase in size of the resulting PSP's is called [] (or sometimes facilitation)
A: potentiation
Q: Often the potentiation persists even after the tetanic simulation. This is called [] potentiation and may last for an hour.
A: post-tetanic
Q: Intrinsic Synaptic Plasticity: in a primitive sense, this is learning. In some neurons, post-tetanic potentiation may last for many hours to days and be specific to certain patterns of input, and is termed [] potentiation (or LTP)
A: long term
Q: The mechanism for post-tetanic potentiation is the accumulation of [] in the terminal .This implies that normally there must be some [] pump removing residual [] from the terminal.
A: Ca++
Q: There are factors outside the neuron that can influence the entry of [] into the terminal. Until now, we have been dealing with axons that terminate on hte dendrites and soma of other neurons, so called "axo-somatic" and "axo-dendritic" synapses.
A: Ca++
Q: Now we must consider neurons that have axon branches that terminate on the terminals on other neurons, referred to as "[]" synapses
A: axo-axonic
Q: Neurons that [] onto the soma and/or the dendrites of another neuron will influence the initiation of an action potential in the taget neuron
A: synapse
Q: Neurons that synapse onto the terminal of another neuron will influence the VlowerM at the terminal and thus will influence the amount of Ca++ influx and ultiamtely influence the amount of transmitter released and the size of the []
A: PSP
Q: The axo-axonic synapse causes the terminal to [] or to hyperpolarize depending on the transmitter-receptor interactions. Not that an axo-axonic synapse will not generate an [] potential.
A: action
Q: The process whereby an axo-axonic synapse [] the amount of transmitter substance that is released is called presynaptic inhibition
A: reduces
Q: The process whereby an axon-axonic synapse [] the amount of transmitter substance that is released is called presynaptic facilitation
A: increases
Q: Presynptic inhibition is thought to be mediated by: 1. the simultaneous closing of Ca++ channels and the of [] channels (via a second messenger system)
A: K+
Q: Presynptic inhibition is thought to be mediated by: 2. an increased [] conductance
A: Cl-
Q: Presynptic inhibition is thought to be mediated by: 3. direct inhibition of neurotransmitter release indpendent of []
A: Ca++
Q: Presynaptic facilitation is though ot be mediated by enhanced Ca++ influc as a result of closing [] channels
A: K+
A: ligand
Q: []-synaptic receptor/channel is the transmitter/receptor binding that activates the gate.
A: Post
Q: All chemical sensetive channels have two common features: 1. they are membrane spanning proteins; AND the region exposed to the [] environment recognizes and binds neurotransmitter molecules;
A: external
Q: All chemical sensetive channels have two common features: 2. they mediate an "[]" function of changing the conformation of an ion channel
A: effector
Q: Receptors that bind neurotransmitter molecules fall into two categories: 1. receptors that gate ion channels [] (ionophoric channels)
A: directly
Q: Receptors that bind neurotransmitter molecules fall into two categories: 2. receptors that gate ion channels [] (metabophoric channels)
A: indirectly
Q: There are some important differences between direct [] sensetive channels and indirect [] sensetive channels.
A: chemical
Q: Chemical Sensitive Channels - direct vs. indirect: 1) In receptors that gate ion channels directly the recognition site and the channel are one unit. Receptors that gate ion channels [] have these components separate, thus the presence of transmitter must be conveyed by a second system
A: indirectly
Q: Chemical Sensitive Channels - direct vs. indirect: 2) They have different overall functions. The direct channels produce fast synaptic action (in milliseconds). The indirect produce slow synaptic action (on the order of seconds to minutes) which can modulate activity and is suited for "[]".
A: learning
Q: Chemical Sensitive Channels - direct vs. indirect: 3) Structurally, the direct channels are made up of multiple [] subunits; whereas the indirect channels are (like potential sensetive channels) made up of one long amino acid sequence.
A: independent
Q: Chemical Sensitive Channels - direct vs. indirect: typical [] chemical sensitive channels are found the nerve-muscle synapse that uses acetylcholine (ACh); and in the CNS, those synapses that use glutamate,glycine, gama-amino butyric acid (GABA), ACh, and a set fo serotonin (5HT) receptors
A: direct
Q: Chemical Sensitive Channels - direct vs. indirect: typical [] chemical sensitive channels are found in the CNS in those synapses that use norepinphrine (NE), dopamine (DA) and most synapses that use serotonin (5HT)
A: indirect
Q: Chemical sensetive channels usually are categorized by the specific [] that binds to it and not by the outcome of this binding (i.e. whether it is an EPSP or an IPSP)
A: neurotransmitter
Q: Within each general class of neurotransmitter sensitive receptor, there are sub-classes of these receptors that can be distingushed by specific agonists that bind to them in addition to the []
A: neurotransmitter
Q: Chemical Sensitive Channels: There are three [] chemical sensitive channels: 1) acetylcholine - ACh 2)y-amino butyric acid - GABA 3) glutamate First ACh receptors.
A: DIRECT
Q: Chemical Sensitive Channels- the ACh receptor: The prototype direct chemical sensitive channel is the ACh receptor. The are [] basics types of receptors for ACh. Both bind ACh and each exclusively bind a certain agonist (and antagonist)
A: two
Q: Chemical Sensitive Channels- the ACh receptor: One type of ACh receptor binds nicotine and is called the ACh -nicotinic receptor. The other type of ACh receptor binds [] and is called the ACh-muscarinic receptor.
A: muscarine
Q: Chemical Sensitive Channels- the ACh receptor: The ACh - nicotinic receptor, which is the one in the nerve-muscle synapse, is the direct ACh receptor. It is a glycoprotein formed by five subunits: the Alpha, Beta, Gama and Delta subunits. The are [] alpha subunits
A: two
Q: Chemical Sensitive Channels- the ACh receptor: only the [] surface of the alpha subunit binds ACh and for the channel to open you need two ACh molecules binding to each of the alpha subunits
A: exterior
Q: Two ACh molecules one on each alpha. no binding - channel []
A: closed
Q: Chemical Sensitive Channels- the ACh receptor: Each subunit has 4 a-helical strings of 20 amino acids that go through the membrane (referred to as M1-M4). The [] section of each subunit is the region that lines the actual lumen of the channel.
A: M2
Q: It is the [] region that is on the lumen side of each subunit
A: M2
Q: Chemical Sensitive Channels- the ACh receptor: There are [] rings of negative charge in the lumen of the channel, actually in the M2 regions. This may serve as some sort of ion selector.
A: three
Q: Chemical Sensitive Channels- the ACh receptor: The actual shape of this ACh [] receptor appears to have a wide funnel type "mouth" on the external side, then it narrows for the probable selectividy site, and then widens again inside the neuron
A: nicotinic
Q: Chemical Sensitive Channels- the ACh receptor: The ACh receptor causes an [] and actually allows both Na+ and K+ to flow through its channel. To accomplish this the lumen has to larger than the potential sensitive voltage gated channels for either Na+ or K+
A: EPSP
Q: Chemical Sensitive Channels- the GABA receptor: The GABA(A) receptor has five sub-units, made up of three different types: alpha, beta and gamma subunits, with 2 alphas and 2 betas. The GABA receptor allows [] flux and will therefore cause IPSP's and be an inhibitory influence.
A: Cl-
Q: Chemical Sensitive Channels- the GABA receptor: All four sub-units of the GABA(A) receptor binds GABA but the alpha subunit is best (has the highest affinity). The [] subunits also binds benzodiazepines, (diazepam- valium, triazolam - halcion, etc.)
A: gamma
Q: Chemical Sensitive Channels- the GABA receptor: The beta (and alpha) subunit also binds [] (phenobarbital, secobarbital, pentobarbital, etc.). The presence of one ligand binding will influence the binding of the others.
A: barbiturates
Q: Chemical Sensitive Channels- the GABA receptor: The outcome of GABA receptors binding benzodizepines is to increase the affinity/efficiency of the GABA receptor to bind GABA. The GABA receptor ocilates between low and [] affinity for GABA.
A: high
Q: Chemical Sensitive Channels- the GABA receptor: Benzodiazepines binding to GABA receptors will keep the affinity of the GABA receptors high. Benzodiazepines themselves DO NOT open the [] channel of a GABA receptor.
A: Cl-
Q: Chemical Sensitive Channels- the GABA receptor: It is not clear how the barbiturates effect the efficiency of the GABA channel. Note the barbiturates exerts effects on tissue that does not have GABA [].
A: receptors
Q: Chemical Sensitive Channels- the GABA receptor: The book mentions how GABA and ACh and glycine channels are similar even though GABA and glycine are anion selective and ACh is cation selective. They are similar: 1) genes that encode them are from the same family. All these subunits are very [].
A: similar
Q: Chemical Sensitive Channels- the GABA receptor: The book mentions how GABA and ACh and glycine channels are similar even though GABA and glycine are anion selective and ACh is cation selective. They are similar: 2) each subunits has [] membrane spanning helical structures (M1-M4)
A: 4
Q: hemical Sensitive Channels- the GABA receptor: The book mentions how GABA and ACh and glycine channels are similar even though GABA and glycine are anion selective and ACh is cation selective. They are similar: 3) the M2 member of each subunit is the channel lumen. In the case of GABA and glycine, the M2 member has clusters of amino acids that results in a selective sections for anitions; which is not present in the M2 section of the [] channel
A: ACh
Q: Chemical Sensitive Channels - the glutamate receptor: There are four types of glutamate receptor based on particular chemicals that will also bind to it: 1. Kainate receptor - (Kainic acid) 2. quisquilate A - (quisquilic acid) (these two are found on [] neurons especially)
A: motor
Q: Chemical Sensitive Channels - the glutamate receptor: There are three similarities between these two glutamate receptors: a)both are affected by AMPA (alpha-amino-3hydroxy-methyl-isoxazole proprionic acid) b) both are [] affected by NMDA (n-mthyl d-aspartate)
A: NOT
Q: Chemical Sensitive Channels - the glutamate receptor: c) both gated a [] conductance cation channel that fluxes/allows flow of Na+ and K+ but NOT Ca++. Sometimes these first two types are referred to as the "AMPA" types
A: low
Q: Chemical Sensitive Channels - the [] receptor: The rest of the glutamate receptors: 1. Kainate receptor - (Kaininc acid) 2. quisquilate A - (quisquilic acid) 3. quisquiliate B - (g-protein type) 4. NMDA receptor whic has two exceptional proprities
A: glutamate
Q: Chemical Sensitive Channels- NMDA receptors. 1.these receptors gate a [] conductace cation channel that fluxes Na+ K+ and Ca++ ions
A: high
Q: Chemical Sensitive Channels- NMDA receptors 2. these channels are pluggged up by [] Mg++, and the channel wont operate unless the Mg++ is removed (by depolarization)
A: extracellular
Q: Chemical Sensitive Channels- NMDA receptors SO the VM must be sufficiently deplolarized to blow out the [] (around 20-30 mV) AND glycine is necessary
A: Mg++
Q: The greater the depolarization the [] current flow through the NMDA channels
A: more
Q: Chemical Sensitive Channels- NMDA receptors: In neurons with both AMPA (non-NMDA) and NMDA receptors, in normal circumstances EPSP's are due mostly to the activity of AMPA receptor/glutamate interactions, which may be enough to blow out some of the []
A: Mg++
Q: Chemical Sensitive Channels- NMDA receptors: However, if the postsynaptic surface is subjected to many []'s, then the NMDA receptors become increasingly more important. This may be a critical feed-forward system for learning.
A: EPSP
Q: Chemical Sensitive Channels- NMDA receptors: This is a case of "Synaptic Plasticity" due to increases in []-synaptic activity
A: post
Q: Chemical Sensitive Channels- NMDA receptors: In other words if a synaptic is involved in a great deal of [] activity, then events will happen (namely the influx of Ca++) that can mark that particualr synapse
A: sustained
Q: Chemical Sensitive Channels- NMDA receptors: Initially we had discussed "synaptic plasticity" in the context of []-synaptic events, whether at the axon hillock or at the terminal in which case the story was one of []-synaptic Ca++ regulating the amount of neurotransmitter molecules that would be released
A: pre
Q: Chemical Sensitive Channels- NMDA receptors: The NMDA receptor is the prime example of how the []-synaptic can be involved in synaptic plasticity. In this case prolonged EPSP's can intiate events that normally would not occur, including the actual "sprouting" of more dendritic spines !!
A: POST
Q: Chemical Sensitive Channels- NMDA receptors: There is a pharmacological differece between AMPA and NMDA receptor types, in that NMDA receptors are blocked by APV (2-amino 5 phospho-novalerate) and are [] by phencyclidine (PCP-angel dust)
A: inhibited
Q: Chemical Sensitive Channels- NMDA receptors: Imbalance in [] is quite disruptive and may lead to certain disease conditions due to a glutamate toxicity or "excitotoxicity" (maybe due to too much Ca++)
A: glutamate
Q: Chemical Sensitive Channels- NMDA receptors: Degenerative disorders like Huntigton's chorea, Parkinson's disease, stroke in general, maybe even Alzheimer's disease may all be influenced by too much []
A: Ca++
Synthesis and Pathways
A: muscarinic ACH, serotonin (5HT), dopamine (DA), and both alpha and beta noreinephrine (NE) receptors
Q: #4 In these receptors, the recognition of neurotransmitter molecules is done on one structure and the activation of some effector is accomplished by an enzymatic cascade, often involving at least [] enzymes.
A: two
Q: #5 G-proteing chemical sensitive channels have a slow onset (hundreds of milliseconds to seconds) and a longer lasting duration of the postsynaptic effect (seconds to minutes) compared to [] chemical sensitive channels.
A: direct
Q: #6 There are only a few well described G-protein (second messenger) systems: [...] .
A: 1) cAMP 2) Phospho-inositol 3) arachidonic pathway
Q: #7 *G-Proteins - common featarues* There are common features to all the g-protein systems: [...] 3) nuerotransmitter bound to the receptor site on the 7-spnning structure activates a guanosine nucleotide-binding protein otherwise known as the "g-protein" to intitiate the process.
A: 1) The all belong to the same gene family; 2) they all consist of a single subunit that has seven membrane spanning regions
Q: #10 This system proceeds in 2 phases: [...] 2) Phase Two- the second messengers lead to changes in specific proteins within the neuron
A: Phase One- the 1st effector enzyme is activated producing a "second messenger"
Q: #16 *G-Proteins - Phase One* The receptor has a site facing the synapse (outside) that will bind neurotransmitter, and it has a site inside the neuron to bing the [].
A: G-protein
Q: #17 The G-protein has 3 subunits: alpha, beta and gamma. The beta and gamma subunits are closely bound to the internal side of the neuronal [], the alpha subunit is less rightly bound.
A: membrane
Q: #18 The [] subunit has a high affinity for guanosine di-phosphate (GDP) and normally binds a GDP. And it is differences in this alpha subunit that distingushes different G-proteins.
A: alpha
Q: #20 There are 3 basic classes of G-protein: [] which will stimulate adenylate cyclase (b-adrenergic receptors); Gi which will inhibit adenylate cyclase (a-adrenergic and some muscarnic receptors); and Go or G-other because it is not clear what it does.
A: Gs
Q: #21 There are more G-other receptors in the brain than any other class of []. Go does stimulate phospholipase C.
A: G-protein
Q: #22 Just as different subtypes of receptors can be distingushed by what binds to i, so also can different G-proteins be distinguished by what [] bind to it.
A: toxins
Q: #23 [] is permanently activated by toxin from cholera; whereas Gi and Go are inactivated by the toxin from the whooping cough bacterium (bordetella pertussis).
A: Gs
Q: #25 *Activating G-Protein Systems" To activate a "G-Protein" system: 1. The process begins when an agonist (usually the neurotransmitter molecules released from the presynaptic surface) interacts with the [].
A: receptor
Q: #27 When the receptor binds transmitter it increase its affinity for the []
A: G-protein
Q: #28 This agonist-receptor complex draws the G-Protein (along with its attached GDP) and forms an agonist-receptor-G-Protein []
A: complex
Q: #30 This agnonist-receptor-G-Protein complex causes the [] sub-unit to exchange its GDP for a high energy GTP, the G-Protein then "dissociates" (explodes);
A: alpha
Q: #31 The combination of the receptor and transmitter and G-protein cause the exchange of the GDP for a [].
A: GTP
Q: #32 The presence of the high energy [] causes it to explode !
A: GTP
Q: #33 *G-Proteins Phase One* The charged-up alpha subunit will now activate the "1st effector" enzyme. This is how they all start and the specific 1st effector enzyme is what distinguishes the various []
A: G-proteins
Q: #34 @G-Proteins Phase One -Summary@ 1) receptor binds neurotransmitter 2) the receptor/neurotransmitter complex draws and binds the G-protein with its attached GDP 3) the receptor/neurotransmitter/G-protien complex causes the exchange of GDP for a high energy []
A: GTP
Q: #35 4)the whole complex "dissociates" (i.e. explodes) 5) the [] subunit has the GTP and can now activate the 1st effector enzyme
A: alpha
Q: #36 It is important to note that G-proteins outnumber receptors. So that a single neurotransmitter/receptor binding can yield many charged-up [] subunits. So G-protein systems can "amplify" a smallish release of neurotransmitter.
A: alpha
Q: #37 @G-Proteins- The 1st Effector Enzyme@ For the c-AMP system the 1st effector enzyme is adenylate cyclase. For the inositol system it is phospholipase C (PLC). For the [] system it is phospholipase A.
A: arachidonic
Q: #38 The activation of the individual 1st [] enzymes produces "second messengers" and starts the next phase of the provess - "second messenger-induced changes in specific proteins"
A: effector
Q: #39 @G-Proteins Phase Two - Overview@ Changes in specific proteins can be accomplished by either 1) the second messenger directly binds to the target protein; OR 2) the second messenger directly activates a 2nd effector enzyme, typically a protein kinase that adds [] groups to a protein
A: phosphate
Q: #40 Among the many consequences of adding phosphate groups (PO4) to a protein are: 1) altering the conformation of an enzyme which then modify the [] of that enzyme; 2)altering a cytoskeletal protein -changing the shape of a structural protein like a channel
A: function
Q: #41 3) altering those proteins that regulate [] transcription
A: DNA
Q: #42 These changes that happen depend on the actual/absolute concentrations of [] messenger and can last for seconds or even minutes
A: second
Q: #43 The [] of the changes is directly limited by the other enzymes that 1) inactivate the second messenger (usually by changing their shape) 2) remove the phosphate groups added onto the target protein
A: duration
Q: #44 These enzymes are always present and active and provide a constant counter to the effects of the 1st and 2nd [] (namely the effects of synaptic transmission)
A: messengers
Q: #45 @Activating G-Protein Systems@ 4. the high energy [] sub-unit activate the normally inactive Adenylate Cyclase 5. the activated adenylate cyclase converts ATP to cAMP
A: alpha
Q: #46 @the cAMP G-Protein System@ The cAMP system is the best studies of all of these systems and remaing the prototype. We pick up the action with the [] subunit all charged up and ready to stimulate adenylate cyclase.
A: alpha
Q: #47 When activated by the charged-up alpha subunit, adenylate cyclase, which is the 1st effector enzyme, will convert ATP (which is abundant in the cell) to cyclic AMP or []. [] is the second messenger.
A: cAMP
Q: #49 cAMP in turn activates cAMP-dependent protein kinase. It does so by attaching to a portion of the protein kinase called the regulatory subunit (R). Le'ts examine protein [] in general.
A: kinases
Q: #50 6) the cAMP in turn activates and otherwise inactive Protein Kinase; 7)the activated Protein Kinase then adds [] groups to the channel
A: phosophate
Q: #51 @Protein Kinases@ Therea are three protein kinases that will concern us: 1) cAMP-dependent kinase 2) protein kinase [] 3) Ca++/ calmoduling-dependent protein kinase
A: C
Q: #52 For all of these, there are functional similarities: 1) there is a "catalytic" subunit which essentially is the portion of he enzyme that does the work; ) there is a "regulartory" subunit whose role is to prevent the [] part access
A: catalytic
Q: #53 This is done by the regulatory subunit globbing onto and thereby covering the active sites of the catalytic subunits. THere is a region on the regulatory subunit that serves as a "pseudo-substrate" and structurally resembels [] substrate but nothing happens when it attaches
A: normal
Q: #54 To get the catalytic subunit to operate, one must remove the regulatory subunit and allow the nnatural substrates access to the sites on the [] subunit so the enzyme can perform its function
A: catalytic
Q: #55 In the case of cAMP-dependent protein kinase, the regulatory and catalytic subunits are separate of two. It takes [] cAMP molecules attached to the regulatory subunit to cause it to separate.
A: two
Q: #57 [] subunits are inactive because thier active sites are covered.
A: catalytic
Q: #59 In the case of protein kinase [] and Ca++/calmoduling dependent protein kinase, the regulatory and catalytic subunits are parts of one strucutre that folds over on itself, not unlike a jack knife.
A: C
Q: #60 To activate these enzymes requires that the strucutre unfol thereby exposing the active sites on the [] subunit. back to the cAMP system
A: catalytic
Q: #64 @the CAMP G-Protein System@ After cAMP has "activated" the cAMP-dependent protein kinase, this protein kinase will then add [] groups (PO4) onto the cannnel.
A: phosphate
Q: #65 The presensce of phosphate groups or the channel will cause a change in the confirmation of the channel which may result in the channel opening if it is normally closed and ions flowing thorugh OR May result in closing a normally [] channel
A: open
Q: #67 @Activating G-protein systems@ The presence of [] groups on the channel will cause a change in the confirmation of the channel in this case resulgin in the channel opening and ions flowing through
A: phosphate
Q: #68 Now remember that there are other enzymes that are always present and always active that will try to keep the post-synaptic are at a basal - pre-action [] condition
A: potential
Q: #69 @the cAMP G-Protein System@ A synapse has to return to a pre-action potential state quickly to be able to receive the next action potential. Let's examine these special "de-activating" enzymes in the [] system
A: cAMP
Q: #70 @De-activating G-Protein Systems@ 1. One enzyme will remove the phosphate groups from the channel that the activated protein kinase added thereby returning it to the basal condition. This enzyme is []
A: phospho-protien phosphatase
Q: #72 Another enzyme will convert cAMP to ADP. ADP cannot activate protein kinase. Thie enzyme is []. This enzyme thus removes the stimulus that activates any further protein kinase activity.
A: phosophodiesterase
Q: #73 In addition, when the charged-up alpha subunit is bount to the adenylate cyclase, it (the alpha subunit) has GTPase activity, which means that it will convert its attached GTP to []. This it stops istself and thereby removes the stimulus for adenylate cyclase.
A: GDP
Q: #74 The [] subunit with GDP attached instead of GTP will dissociate from the adenylate cyclase (ending the production of cAMP) and the will re-associate with the beta and gamma subunits.
A: alpha
Q: #76 Finally, and independent of these other activities, the neurotransmitter is removed from the [] site thus ending the stimulus that starts the whole process. (removing the stimulus for the formation of a charged alpha-sub-unit).
A: receptor
Q: #77 It is important to remember that these various processes, especially the "[]" ones, do not occur in a linear
A: deactivating
Q: #78 @The Inositol G-Protein Systme@ Another G-protein systme is the "Phosohatidyl inositol" (PI) or simply just "inositol" system. It is similar to the [] systme in that the intial phase of getting a charged alpah subunit is the same. However, the rest of the process is very different.
A: cAMP
Q: #79 The 1st effector enzyme is phosphlipase C (PLC). When activated by the alpah subunit, PLC will produce [] second messengers: 1) diacyglcerol (DAG; and 2) inositol triphosphate (IP3)
A: TWO
Q: #81 There is a membrane lipid- phosphatidyl inositol (PI). Activated phosphlipase C will cleave the fatty acid chains that keep the inositol triphosphate bount to the []
A: membrane
Q: #82 The cleaving of PI leaves one protion- DAG- that is hydrophobic and remains in the lipid middle of the membrane; and the other portion -IP3- that is water soluble can go into the cytoplasm/ inside the []
A: neuron
Q: #84 Each of these [] messengers has its own protein kinase to activate. But these two pathways are different from one another and diferent from the cAMP system. Let's follow the IP3 branch first.
A: second
Q: #85 @the Inositol G-Protein System -the IP3 branch@ These are the general steps of the IP3 branch: 1) once phosphlipase [] causes the release of IP3 in the postsynaptic side, IP3 moves into the cytoplasm and binds to receptos in the endoplamic reticulum
A: C
Q: #86 2) IP3 binding to ER receptors causes the release of [] from ER stores in to the cytoplasm
A: Ca++
Q: #87 This increase in intracellular [] can do many things, one is to bind yet to another intracellular protein called "calmoduling: anf form a "Ca++/calmodulin" complex
A: Ca++
Q: #90 3) there is a protein kinase that is sensitive to (i.e. is activated by) Ca++/calmoduling and it is called "Ca++/ calmoduling dependent protein kinase. 4) when activated, thie protein kinase will then add [] group to target protein
A: phosphate
Q: #93 @the Inositol G-Protein System- the DAG branch@ The portion of the PI that remains trapped in the membrane after the action of PLC is DAG. This free protion activates protein kinase [] which can the add phosphate groups to the target protein.
A: C
Q: #94 The interesting twist with the DAG branch of the inositol system is that protein kinase [] is the cyptoplasm and has to be "translocated" to contact the membrane and have DAG "open" the enzyme.
A: C
Q: #95 the "closed" PKC is translocated to [] and then it "opens"
A: DAG
Q: #97 @the Inositol G-Protein System@ It is important to note that the [] second messengers produced by PLC can act independently as well as synergistically.
A: two
Q: #98 @Special Issues@ There are five special issues concerning G-protein systems: 1) G-protein systems can interact with one another 2) G-proteins often will open OR close [] channels (via protein phsophrylation)
A: ion
Q: #99 G-proteins can sometimes act directly on ion channels (that is not via phosphorylation); 4) G-proteins can alter the propreties of transmitter receptors (called "desensitization) 5) G-proteins can regulate [] expression
A: gene
Q: #100 @G-proteins often will open OR close ion channels@ Just like directly gated chemical sensetive channels, G-protein systems can open normally closed ion channels. G-protein systems can also [] channels that are normally open, and the case if not-gated/passive K+ channel is a special example
A: CLOSE
Q: #101 Just like directly gated chemical sensitive channels, G-protein systems can open normally closed ion channels
Q: #102 In certain cells, some non-gated [] channels are controlled by synaptically activated G-protein systems. Closure of non-gated [] channels increase the excitability of the postsynaptic neuron and prevents accomodation to repetitive AP's
A: K+
Q: #103 The close of channels by G-protein systems is nor restricted to non-gated channels. Some potential senitive (voltage gated) channels can also be closed by G-protein system. An example is NE and enkephalin in dorsal root ganglion cells close potential sensitive [] channels
A: Ca++
Q: #104 The time course of these enhanced excitability action of G-protein systems is much slower than the actions of direct chemical sensitive channels that also produce []
A: depolarization
Q: #105 Leutinizing hormone releasing hormone (LHRH) is a peptide G-protein system that induces a very slow []
A: EPSP
Q: #106 @G-proteins can sometimes act DIRECTLY on ion channels@ In some cases, the alpha subunit can directly act on the ion channel causing the channel to change conformation. This action is [] of any subsuquent phosphorylation.
A: independent
Q: #107 In addition, second messengers themselves can also function this in this manne. In some cases, the [] subunit may have a similar direct effect. These reacations are fast and are added to the phosphorylation effects that also occur.
A: beta
Q: #109 @G-proteins can alter neurotransmitter receptors@ Ion channels need not be the only [] structure that are the "target proteins" for G-protein systems. The actual neurotransmitter receptor, whether direct or indirect, can also be a target protein.
A: protein
Q: #110 Thus, the action of one receptor can regulate not only its own effectiveness but also the effectiveness of other receptors. Recall that [] messengers can diffuse within the postsynaptic surface for some distance.
A: second
Q: #112 @G-proteins can regulate gene expression@ With repeated activation, a G-protein system can activate protein kinase to such a high level that it will phosphrylate transcriptional protein in the nucleus of the neuron that will lead to the production of [] proteins.
A: new
Q: #114 @NEUROTRANSMITTERS@ We have seen not only how neurons communicate but more importantly the [] in this communication so that a variety f outcomes can happen depending on the circumstances
A: plasticity
Q: #116 Now we should consider the last major theater of neuronal plasticity- neurotransmitter []
A: synthesis
Q: #117 The book breakdown of neurotransmitter classes are: [...].
A: 1.Acetycholine (ACh) 2. the Biogenic Amines 3. the Amino Acids 4. Neuroactive Peptides
Q: #118 The Biogenic Amines are [...]
A: 1. Dopamine (DA) 2. Norepinephrine (NE) 3. Serotonin (5HT) 4. Histamine
Q: #119 The Amino Acids Neurotransmitters are:
A: 1. gamma aminobutyric acid (GABA) 2.Glutamate 3. Glycine
Q: #122 The Neuroactive families: 1. pro-opio-melanocortin (POMC), in which group is beta-[] 2. pro-enkephaling, in which group are met-, and leu-enkephalins 3. pro-dynorphin, in which gorup is dynorphin
A: endorphin
Q: #124 There are 4 criteria for calling a substance a neurotransmitter: 1. it must be synthesized in the neuron 2. it must be released in sufficient amounts upon an AP to yeld []'s
A: PSP
Q: #125 3. exogenous applications will mimic normal activity 4. there must some [] mechanism(s) (some way of terminating the transmitter-receptor interaction)
A: deactivating
Q: #126 []'s law state that a mature neuron makes use of the same neurotransmitter in all of its synapses. But neurons have been shown to release more than on transmitter so the new []'s law is as follows:
A: Dale
Q: #127 A mature neuron makes use of the same combination of neurontransmitter substances in all of its synapses. The use of more than one transmitter by a neuron is called "[]"
A: coexistance
Q: #128 For all the neurotransmitters you shoud know the 1. synthesis pathway (as well as any regulatory enzymes) 2. the [] systems which may be in both the pre-synaptic and post-synaptic surfaces
A: deactivating
Q: #129 For all the neurotransmitters, except the neuroactive peptides, the synthesis occurs for the most part in the []-synaptic axon terminal where the product of this synthesis is packaged in the vesicles. We begin with acetylcholine (ACh)
A: pre
Q: #130 @Neurotransmitters-Ach@ Acetyl Co-enxyme A and Choline -----(Choline Acetyl Transferase (CAT))------> [] (ACh)
A: Acetylcholine
Q: #131 note: 1) the [] CoA is furnished by normal glucose metabolism and 2) choline is brought in from Blood and the cleft
A: acetytl
Q: #132 Choline is borught into the cell from dietary sources. The deactivating mechanism is the enzyme Acetylcholinesterase (ACHE) which exists in the synapse next to the ACh receptor (and AChE exists in the [])
A: terminal
Q: #133 For acetylcholine, the de-activating mechanim is the presence of ACHE right next to the receptor. So when the ACH spontaneously unbinds from the receptor, AChE is there to break the [].
A: ACh
Q: #135 Acetylcholinesterase (AChE) breaks down ACh at the synapse very quickly and yeslds acetate and choline. This is a special transport mechanism in the pre-synaptic membrane that has a hgih affinity for []
A: choline
Q: #136 This transport gizmo is a protein that has an external face into the synaptic cleft. It will bind choline molecules and then pill them back into the terminal. Thus the choline is recycled to be used in the synthesis of [] over and over again.
A: ACh
Q: #139 The acetylcholinesterase (AChE) that exists in the []-synaptic terminal is especially important. []-synaptic AChE breaks up any ACh that has not bound to or has been taken into a vesicle.
A: pre
Q: #140 This raises three critical issues tha apply to all the other transmitter systems as well: 1) the vesicles are essentailly "safety zones" which protect the transmitter molecules from being broken down by []; and
A: enzymes
Q: #141 2) the vesicles are not saturated, that is ,they are not normally filled to capacity 3) how do neurotransmitter molecules get into the vesicle. The filling of the vescile then becomes an important point of []
A: plasticity
Q: #142 @Neurotransmitters- Vesicle Transporters@ Vesicle have the capacity to accumulate and store high concentrtation of neurotransmitter molecules. There are [] vesicular membrane mechanisms involved: the transmitter transporters and a proton pumper.
A: two
Q: #144 The purpose of the proton pumper is to keep the inside of the vesicle supplied with []. Thes creates an electrochemical source for the transmitter transporter.
A: protons
Q: #145 The vesicle exchanges 2 protons for every molecule of neurotransmitter brought in. There are [] distinct vesicular transmitter transporters that have been defined.
A: 4
Q: #146 Transmitter transporters: One for Ach, one for the biogenic amines (VMAT), one for glutamate and one for []. These transporters are different from the cell membrane transporters like for choline uptake.
A: GABA
Q: #147 The Monamines are
A: 1. the Catecholamines: Dopamine (DA) ; Norepinephrine (NE) 2. the Indoleamines: Serotonin (5HT)
Q: #148 For the Catecholamines: Dopamine (DA) Norepinephrine (NE) the synthesis pathway is [] :
A: similar
Q: #149 tyrosine ----via tyrosine hydroxylase--> L-DOPA ---via dopa decarboxylase--> []
A: Dopamine
Q: #151 The rate limiting enzyme for this CA synthesis is the first enzyme - tyrosine hydroxylase. Tyrosine hydroxylase exists in an [] form and needs a pterdine cofactor to become active
A: inactive
Q: #152 tyrosine----via tyrosine hydroxylase (<-- pteridine cofactor) ----> []
A: L-DOPA
Q: #155 Actually, the pteridine is tetra-hydro-pteridine (pteridine-H4) and contributes hydrogens to tyrosine hydroxylase to make it []. Once having contributed two hydrogenc, pteridine becomes di-hydro-pterdidine (pteridine-H2).
A: active
Q: #156 There is another enxyme - pteridine reductanse that will add [] back to ptrerodome to get it back to pteridine-H4 and able to activate tyrosine hydroxlase.
A: hydrogens
Q: #157 tyrosine ----via trysoine hydroxylase*--> L-DOPA ----via dopa decarboxylase---> [] *: Pteridinic-H4 cofactor --->pteridinic-H2 cofactor---->Pteridine reductase--->Pteridinic-H4 cofactor
A: Dopamine
Q: #158 They synthesis of norepinephrine (NE) is essentially the same as for DA except that neurons that use NE have vesicles that have one additional [] that converts the DA coming into it to NE
A: enzyme
Q: #159 tyrosine ----via trysoine hydroxylase*--> L-DOPA ----via dopa decarboxylase--->Dopamine---via dopamine beta hydroxylase-->[]
A: Norepinephrine
Q: #160 The main de-activating mechanism for all [] monoamines is a process called "re-uptake", which draws the moelcules into the presynaptic and the postsynaptic sides. This is done by membrane transporters.
A: three
Q: #161 @Neurotransmitters- Membrane Transporters@ There are two general classes of membrane transporters: 1) transporter for Glutamate; 2) transporters for GABA, glycine, norepinephrine, dopamine, serotonin, and []
A: choline
Q: #162 These two transporters are similar in that : 1) they are both driven by the [] concentration gradient; 2)they both co-transport another ion
A: Na+
Q: #163 These two transporters are dis-similar in that: 1) the Glutamate transporter is made up of a protein that spans the membrane 6-8 timesl; and the other transporters spans the membrane [] times;
A: 12
Q: #164 2) the other difference is in the co-transported ion: the Glutamate transporter requires the contransport of K+; and the other transporter requires the contransport of []
A: Cl-
Q: #166 In Glutamate transport: one glutamate molecule and [] Na+ are exchanged fro one K+ and one OH-. In the other transport: one NT molecule is transported along with 3 Na+ and one Cl-
A: 2
Q: #172 Deactivating monoamine synapses: like the uptake of choline in the ACh terminals, this process of reuptake involves a membrane protein that has a [] affinity for the transmitter and will pull back into the terminal or the postsynaptic side
A: high
Q: #173 @Neurotransmitters- the Monoamines@ In addition, there are two enxymes that breakdown []: 1. Monoamine oxidase (MAO) 2. Catechol-o-methyl-transferase (COMT) Both exist in the terminal, and in the postsynaptic side.
A: Catecholamines
Q: #174 In the presynaptic side, both serve the function of breaking down molecules not in vesicles just like the presynaptic AChE did for ACh neurons. Thus, at the termination of a MA synapse there are [] uptake processes.
A: two
Q: #175 There is the reuptake into the terminal (1) and the transmitter molecules have to be then taken up into vesicle (2) otherwise MAO and/or COMT will destory it. Neurotransmitter molecules take up into the [] side do not have a chance to hide.
A: postsynaptic
Q: #176 The synthesis of Catecholamines has two "short term" feedback systems both of which focus on the rate limiting enzyme - tyrosine hydroxylase: 1. Enf Product Inhiibition 2. [] feedback
A: Ca++
Q: #177 In End Product Inhibition, accumulating amounts of dopamine in the presynaptic terminal will [] the activity of tyrosine hydroxylase
A: decrease
Q: #178 [](the "end product") in presynaptic terminal will sut down the activity of tyrosine hydroxylase by converting (oxidizing) pterrdine-H4 to pteridine-H2
A: Dopamine
Q: #179 The accumulation of presynaptic [] is a good indicator of synaptic activity, and [] will directly and indirectly accelerate the activity of tyrosine hydroxylase.
A: Ca++
Q: #180 Thus end product inhibition is a short term Negative Feedback system and [] is a short term Positive Feedback
A: Ca++
Q: #181 There is a long term feedback system for tyrosine hydroxylase. The continued firing of a neuron may cause that neuron's nucleus to produce more tyrosine hydroxylase. This [] in the synthesis of enzymes is called "induction".
A: increase
Q: #182 This process of induction is probably accomplished by autorecptors on the terminal (pre-synaptic side). THese autoreceptors are []-proteins systems.
A: G
Q: #184 Prolonged release of transmitter results in prolonged autoreceptor stimulation. This which prolonged presynptic [] stimulation leads to the activation of a "transcriptional activator protein"
A: cAMP
Q: #185 This "transcriptional activator protein" called [], will specifically go back to the nucleus and activate that portion of the genetic code that will produce more tyrosine hydroxylase molecules
A: CREB
Q: #186 The synthesis of [] (5HT) is not as well understood as for the CA's in terms of rate limiting enzymes and feedback loops.
A: Serotonin
A: 10%
Q: #4 The basic [] disturbance in this disorder is a profound alteration of mood. This alteration can be expressed as a pathologically depressed mood or pathologically elevated or manic mood.
A: behavioral
Q: #5 In the [] mood, the main sx's include a profound (increases or decreases), changes in sleep (either insomnia or hypersomnia), suicidal ideation or thoughts of death.
A: depressed
Q: #6 In the [] mood, the main sx's include feeling of grandiosity, periods of excessive talking, decreased need for sleep, distractibility, and engaging in risky behavior (financial, business, or sexual indiscretions).
A: manic
Q: #7 Is there a general CNS focus for Affective Disorders? The data suggests that the prefrontal cortex just bellow the genu (the "turn") in the Corpus [] may be involved.
A: Callosum
Q: #8 This are has important connections to [] areas and the lesion data indicates taht people with damage here have their emotional behavior compromised
A: limbic
Q: #9 In the late []s there serendipitous findings that were pivotal in forming working models of Affective Disorders
A: 1950
Q: #11 The drug, iproniazid, was developed and was being used to treat tuberculosis when it was noticed that the patients receiving iproniazid had thier mood elevated to the point of [].
A: euphoria
Q: #12 Hypertensive patients had been given a drug called reserpine that seem to cause these otherwise normal patients to experience profound [].
A: depression
Q: #13 When the findings were released that another suspected antihistamine, chlorpromazine, actually had antipsychotic effects, impramine was tested agains in 1958, and found to have [] activity.
A: antidepressant
Q: #14 Iproniazid was a Monoamine [] Inhibitor (MAO-I); reserpine binds to the vesicles in monoamine terminals and prevents transmitter molecules from entering/binding
A: Oxidase
Q: #15 SO, iproniazid enhanced MA functioning and it elevated mood. [] decreased MA functioning and it depressed mood.
A: resperpine
Q: #16 Other data indicated that [] which also elevate mood and activity levels, enhances MA functioning in three ways
A: amphetamines
Q: #17 @Amphetamine's CNS Actions@ 1. it blocks the reuptake of all [] MA's 2. it enhances release of MA's (probably due to its MAO-I activity) 3. it directly stimulates the postsynaptic receptors
A: 3
Q: #18 @Stimulants' CNS Actions@ Methamphetamine is similar to amphetamine, presumably sharing the same mechanisms, with the exception that it has [] peripheral activity and more central or brain activity than amphetamines
A: less
Q: #19 Cocaine and methylphenidate (ritalin) also block re-uptake of [] neurotransmitters. However, it has not been shown that these drugs share the other actions of amphetamines.
A: monoamine
Q: #20 @affective disorders@ These data bases combined led to the clinical model that affective disorders were a [] "imbalance" or at least that [] transmission was the root pathology in affective disorders. Drug strategies to treat affective disorders emerged.
A: monoamine
Q: #25 @Monoamine Pathways@ The catecholamine nuclei (namely the nuclei of Dopamine and Norepinephrine) have been designated with the notation of A1 through [] and serotonin nuclei as "B" nuclei based on fluorescence data.
A: A13
Q: #26 Norepinephrine (NE). NE nuclei are clustered: 1. A1 through A4 in the []encephalon; 2 A5 through A7 in the Met-encephalon
A: Myel-
Q: #28 Norepinephrine (NE) By far the "star" of the NE system is [] or the locus coeruleus which lies on the dorsal part of the met-encephalon. 43% of all brain NE producing neurons are in locus coeruleus
A: A6
Q: #31 Locus Coeruleus projects to many nuclei via two systems: 1) the "dorsal bundle" or the "dorsal tegmental bundle" and 2) the "ventral bundle" or the "[] tegmental tract"
A: central
Q: #32 THe "dorsal bundle" projects to hypothalamus, septum, hippocampus, amygdala, olfactory bulb, cerebral cortex, central gray, cerebellum, and reticular formation !!! This system is []
A: uncrossed
Q: #33 These NE pathways contribute to the "medial [] bundle" (MFB) which is principle mechanism for "positive reinforcement" or pleasure
A: forebrain
Q: #35 Serotonin (5HT). B1 through B3 are []-encephalic and project to the spinal cord; B4 through B6 are met-encephalic and project to the cerebellum clearly starts of the 5HT system are B7 through B9
A: myel
Q: #36 B7 through B9 are called the "raphe" nuclei; they are []-encephalic. B7 and B8 project to the hypothalamus, septal area, hippocampus, and cerebral cortex (especially the cingulate). These fibers travel in the MFB.
A: mes
Q: #40 @Affective Disorders - Medications@ Basically there are three classes of drugs used to treat affective disorders: 1) the traditional tricyclic antidepressant; 2)the monoamine oxidase inhibitors (MAO-I's); 3) the newer " [] antidperessants"; and 4) lithium
A: heterocyclic
Q: #41 @Affective Disorders- TCA's@ There are TCAs (desipramine, and protriptyline) that block the reuptake of norepinephrine (NE) much more efficiently than they block the reuptake of [] (5HT)
A: serotonin
Q: #42 Whereas there are TCAs (imipramine, amitriptyline, doxepin, clomipramine) that block the reuptake of serotonin (5HT) much [] efficiently than they blcok the reuptake of (NE)
A: more
Q: #43 @Affective Disorders- Medications@ 2. Monoamine [] Inhibitors (MAO-I's) - tranylcypromine (parnate) 3. Heterocyclic Antidepressants- (Specific Serotonin Re-uptake inhibitors) tranzadone, fluoxetine (prozac), sertraline (zoloft), paroxetine (paxil)
A: Oxidase
Q: #44 @Affective Disorders- Monoamine Theory@ The Monoamine theory of Affective Disorders holds that Affective Disorders are the result of either an underactive monoamine system in the brain, OR that the levels of monoamine neurotransmitter molecules in the brain are too []
A: low
Q: #45 The major shortcoming of this theory is that it fails to explain why there is a 10 to 14 day delay from the onset of taking medication and the onset of [] improvement
A: clinical
Q: #46 @Affective Disorders- Beta Adrenergic Theory@ The Beta-Adrenergic Theory of Affective Disorders states that Affective disorders are the result of too many active Beta-adrenergic []
A: receptors
Q: #47 There are two specific receptor types for norepinephrine - the alpha and beta adrenergic receptors. Each has a distinctive distribution in the peripheral nervous system and in the [] nervous system.
A: central
Q: #48 A general characteristics of most receptors and that is not all of them are functional at any one poin in time. A given population of receptors will have a portion that are not active and the brain will regulate how many are [] according to its needs.
A: active
Q: #49 One long term consequence of chronic antidepressant medication is the decreased number, referred to as a down regulation, of [] adrenergic receptors in the brain.
A: beta
Q: #50 This down regulation of beta adrenergic receptors in the brain , which takes approximately 10 to 14 days to accomplish, is found with drugs that block the re-uptake of [], and with a variety of antidepressants that do not directly alter NE
A: norepinephrine
Q: #51 The specific serotonin re-uptake blcokers, like fluoxetine (prozac), sertraline (zoloft) and paroxetine (paxil), also cause the eventual down regulation of [] adrenergic receptors in the brain, as do the MOA-I's and even the non-pharmacological treatment ECT
A: beta
Q: #52 @Affective Disorders - Role of Serotonin@ Recent research has been describing the precise role of [] in the clinical effectiveness of antidepressants
A: serotonin
Q: #53 [] antidepressants will also influence serotonin receptor sensitivity on the cerebral cortex, especially one specific type of serotonin receptor - the 5HT1A
A: Tricyclic
Q: #54 It appears that the serotonin-norepinepherine interaction that may mediate the clinical relief of antidepressant medications is a down regulation of the beta-adrenergic receptor and an [] in serotonin receptor activity
A: increase
Q: #55 Post-mortem biochemical analyses of the brains of suicide victims indicate that the prefrontal cortex has [] levels of 5HT transport activity and higher beta-adrenergic receptor binding.
A: lower
Q: #56 By hampering the 5HT transporter, the SSRI's will alter 5HT transmission. Now the focus has turned to the specific 5HT [] that may be involved.
A: receptors
Q: #57 The key to this line of research is the distribution of the 5HT transporters and of this specific 5HT receptor - the 5HT1A autoreceptor. 2 week delay may be due to the subsequent [] of 5HT release in the forebrain which is mediated by 5HT1A (autoreceptors)
A: inhibition
Q: #58 There is a dense distrubution of the 5HT transporter on the soma/cell body of the serotonin cell as well as on the terminal (in the synapse). Thus, another important target for SSRI's is the [] body of 5HT neurons.
A: cell
Q: #59 If there is a hampering of the 5HT transporter then there will be a driving of any 5HT receptor on the soma as well. The 5HT1A receptor on the soma is an inhibitory autoreceptor. When activated this 5HT autoreceptor will reduce not only electircal activity byt also [] activity.
A: metabolic
Q: #60 There is a bipolar effect to SSRI's on 5HT levels: first there is an [] in 5HT in the forebrain as a result of the transporter hampering, but then that effect is attenuated by driving the 5HT1A's to shut down the 5HT cell
A: increase
Q: #61 @Affective Disorders - Herbal Medications@ Many studies have demonstrated that St. John's Wort - hypericum provides a safe and effective treatment for patients with mild to moderate []
A: depression
Q: #62 @Affective Disorders - St. John's Wort - Hypericum@ Hypericum extracts inhibited both [] and norepinephrine uptake in a dose-dependent manner (it was stronger for NE than for 5HT).
A: serotonin
Q: #63 The data suggest an upregulation of 5-HT1 A and 5-HT2 A receptors due to prolonged administration of [] extracts.
A: hypericum
Q: #64 Hypericum extract inhibits the synaptosomal uptake of serotonin, norepinephrine, and dopamine and leads to a significant down-regulation of cortical beta-adrenoceptors and 5-[]-receptors
A: HT2
Q: #65 Hypericum also exerts a weak inhibition of MAO , and catechol O-methyltransferase. There has also beein a demonstration of [] receptor (an opiate receptor) binding of hypericin
A: sigma
Q: #66 It has been postulated that the clinical efficacy of St. John's wort could be attributable to the combined contribution of several mechanisms, each one too [] by itself to account for the overall effect.
A: weak
Q: #67 @Affective Disorders - ECT@ The procedure involves the use of muscle relaxants and anesthesia to prevents bone factures during the convulsions and to prevents the anxiety surrounding the procedure. THe optimal [] schedule is 6-8 treatments every 2 days for 2 to 4 weeks.
A: ECT
Q: #68 Modern ECT is considered safe, and effective with positive response rates as high as []. ECT is believed to induce more rapid relief than the standard 2 week delay of the TCAs which becomes critical when dealing with some suicidal patients
A: 95%
Q: #69 There remains two significant concerns. First, ECT will invariably induce confusion and a loss of memory surrounding the ECT treatment, which becomes progressively [] severe with increased sessions
A: more
Q: #70 Second, without additional pharmacological support, there is an extremely [] relapse rate
A: high
Q: #71 The precise mechanism by which ECT provides clinical relief is not known. However, ECT, like traditional antidepressant medicaiton, does cause a down regulation of beta-adrenergic receptors, and enhances [] sensitivity in the cerebral cortex
A: 5HT
Q: #72 @Affective Disorders - Mania - Lithium@ Typical responses to lithium: relief of [] symptoms; mental dullness; decreased memory and concentration; headache; fatigue
A: manic
Q: #73 There are a variety of effects on brain functioning following lithium. It is not clear which if any of these effects may be the causal factors in the [] patients. Some of the specific effects include:
A: manic
Q: #74 The effects on brain functioning following lithium: decreae brain calcium levels; enhances reuptake of NE and serotonin; [] release of NE; alter the Na+K+ATPase pump
A: reduces
Q: #75 Lithium also inhibits a key enzyme in the inositol G-protein system thereby [] the responsiveness of the neuron
A: reducing
Q: #77 @Depression and Cortisol@ Patients with major depression often are found to have abnormally high levels of ACTH. This leads to an oversecretion of cortisol. THis may be the result of high levels of cortocotropin relesing hormone (CTRH) in the []
A: hypothalamus
Q: #79 In addition, people that are not suffering from [] have feedback loop that will responds to the administration of a synthetic glucocorticoid - dexamethasone
A: depression
Q: #81 @Anxiety Disorders@ A. Panic Disorder B. Generalized Anxiety Disorder C. Post-Traumatic Stress Disorder D. [2]
A: Obsessive Compulsive
Q: #82 @A. Panic Disorder@ These sudden, unexplainable and frequently occuring attacks of terror are relatively short in duration. The symptoms usually include heart palpitations, labored breathing, sweating, dizziness, and intense []
A: depersonalization
Q: #83 [], in particular alprazolam (xanax), and the tricyclic antidepressants, in particualr imipramine (Tofranil) are the most successful medications for this type of anxiety
A: Benzodiazepines
Q: #84 @B. Generalized Anxiety Disorder@ This is a condition of "free floating" anxiety and the symptoms include heart palpitations, shorteness of breath, sweating, upset stomach, diarrhea, muscle tensiion and [], trembling and twitches
A: aches
Q: #85 Both the long and short acting [] have traditionally been the "first line" medication for Generalized Anxiety Disorder
A: benzodizepines
Q: #86 @C. Post Traumatic Stress@ Post Traumatic Stress patients seem to release [] levels of norepinephrine. Drugs that will decrease NE transmission seems to help symptoms
A: high
Q: #87 @D. Obsessive Compulsive@ This disorder is characterized by overwhelming [] to ritualistically repeat some act over and over again (like hand washing, checking that doors are locked, etc.)
A: impulses
Q: #88 The two components of OCD are persistent fearful thoughts and persistent behaviors. One can consider this a motor disorder in addition to an anxiety disorder and so motor areas of the brain my be involved, especially the [] ganglia
A: basal
Q: #92 @Basal Ganglia@ The Basal Ganglia represent the largest collection of subcortical telencephalic neurons. The interneurons are cholinergic and the main projection type (>90%) is GABAinergic. The two best described inputs are from the cerebral [] that uses Glutamate; and from the substantia nigra which uses dopamine
A: cortex
Q: #93 The Basal Ganglia proper is composed of the: 1. the Caudate nucleus 2. the Putamen 3. the Globus [] which has a lateral or external part and a medial or internal part
A: Pallidus
Q: #94 The caudate and the putamen together are referred to as the "corpus striatum" or []; and the putamen and the globus pallidus together are reffered to as the "lenticular nuclei" or as the "pallidum"
A: striatum
Q: #95 The Basal ganglia and the related structures have neurons that use a wide range of neurotransmitters: 1. interneruons in the caudate use acetylcholine (ACh) 2. interneurons in the putamen use []
A: GABA
Q: #96 3. Striatal projections to the globus pallidus use enkepahin and GABA 4, pars compacta input to striatum uses [] (DA) 5. cerebral cortical input uses glutamate
A: dopamine
Q: #97 6. ouput from striatum to substantia nigra uses GABA and substance [] 7. input from the raphe to the striatum uses serotonin (5HT)
A: P
Q: #100 SSRI' have been successful in treating OCD. The specific antidepressant [] has been the most successful medication. Behavioral therapy alone has also been successful.
A: clomipramine
Q: #101 After effective treatment (either pharmacological or behavioral) hyperactivity in the caudate nuclues and the orbital frontal cortex is []
A: decreased
Q: #103 @Psychoses@ The symptoms include: 1) hallucination 2) delusions 3) distrubances of thought, language and communication 4) disturbances of []
A: emotion
Q: #104 The absence of certain normal social and interpersonal behaviors is referred to as "negative signs". And the presence of distinctly abnormal behavior is referred to as "[] signs"
A: positive
Q: #105 @Psychoses- Anatomical Substrates@ There seems to be several lines of research that suggests there are anatomical differences in the brains of psychotics. 1) there seems to be a [] in the blood flow to the globus pallidus (left side)
A: reduction
Q: #107 This suggests a frontal cortex - basal ganglia defecit; 2) the frontal cortex in general does not respond as vigorously; 3) the cortex of the medial temporal lobe is actually thinner and the anterior portion of the hippocampus is []
A: temporal
Q: #108 4) the lateral and [] ventricles are larger meaning there is less tissue there
A: third
Q: #110 These signs are all typically seen in patients with prominent [] symptoms. It seems that the hippocampus, the prefrontal cortex and the basal ganglia for an important cognitive system
A: negative
Q: #111 In addition modles for hallucinogenic behavir may also involve these structures. The loop suggested in Box 60-1 has four basic components: substantia nigra, basal gaglia, thalamus and inferotemporal []
A: cortex
Q: #113 @Psychoses@ The most compelling data deal with the medications that successfully treat psychoses - the first being the []
A: phenothiazinzes
Q: #114 Phenothiazines - (cholrpromazine (thorazine); thioridazine (mellaril); trifluoperazine (sterlazine); fluphenazine (prolixin)) Butyrophenones - haloperidol (haldol) []
A: Clozapine
Q: #115 @Psychoses - Antipsychotic Medications@ All the antipsychotic drugs share a common mechanism of action on the brain - these drugs block [] receptors. The better and individual drug is at blocking [] receptors the more efficient that drug will be in the clinical treatment of psychoses
A: dopamine
Q: #116 The antipsychotic drugs effect the Peripheral Nervous System as well, in two other ways: 1) the block [] (ACH) receptors and 2) that block alpha-arenergic receptors.
A: acetylcholine
Q: #117 @Antipsychotic Medication Behavioral Effects@ Behaviorally, the antipsychotics typically induce a tranquilized state without loss of []. A condition that was originally termed "artificial hibernation" - an indifference to the immediate environment
A: consciousness
Q: #118 The most profound [] effect on these drugs is the relief of psychotic symptoms in disordered patients
A: behavioral
Q: #119 The symptoms that appear to respond well to the antipsychotic drugs include hallucinations, [] delusions, hostility, flat affect , and general withdrawal. Moreove, these drugs also seem to alleviate the primary "core" symptoms like thought disorder and paranoia.
A: acute
Q: #120 THe blocking of alpha-adrenergic receptors results in some distinctive cardiovascular effects like increased heart rate (tachycardia), mild decrease in blood pressure, postural hypotension, and peripheral vasodilation which causes [] hypothermia
A: mild
Q: #121 Peripherally, antipsychotics block the Muscarinic Acetylcholine receptor which is the postganglionic neurons of the Parasympathetic Nervous System. In other words, it antagonizes the Parasympathetic Nervous System. Thioridazine (Mellaril) is the [] potent.
A: most
Q: #122 Centrally, blocking central [] receptors leads to memory difficulties, confusion, and maybe delirium
A: muscarinic
Q: #123 @Antipsychotic Medications Hormonal/Behavioral Effects@ Increased [] release, which leads to hyperprolactinemia. In females, galactorrhea (a continued discharge of milk), decreased frequency of flow in menstruation. In both genders, decreased libido, and delayed, altered, or inadequate orgasms.
A: prolactin
Q: #124 @[] Systems@ 1) the nigro-striatal dopamine pathway - 2) the meso-limbic and meso-cortical systems. This is the target systme for antipsychotic medication. 3) the tubero-infundibular system-
A: Dopamine
Q: #126 @Monamine Pathways@ Dopamine. The dopamine system was once considered to be only a motor system. Its nuclei are more rostral than the NE nuclei. A8 through A10 are in the mes-encephalon; and A11 through A13 are in the []-encephalon
A: di
Q: #128 Dopamine A9 is the "zona compacta" of the substantia nigra. A8 and A9 project to the caudate and putamen as the "nigro-strital pathway". The nigro-strital system contains [] of all brain dopamine.
A: 75%
Q: #129 The nigro-striatal pathway is vital for motor control. There are about 3500 DA cells in zona compacta, and there are about 4 million target cells in the basal ganglia. Each compacta axon collateralizes to form about [] synapses !!!
A: 500,000
Q: #130 The second most prominent DA pathway comes from [] (the interpeduncular nucleus) to form the "mesolimbic" system which projects to nuclues accumbens, amygdala, septum, hippocampus, frontal cortex and cingulate cortex.
A: A10
Q: #131 There are two other DA systems: 1) from [] (the arcuate nucleus) to the conection of the pituitary; 2. internal communications within the hypothalamus
A: A12
Q: #133 @Dopamine Systems@ The Weinberg model is proposed in the reading. It states that the meso-[] portion of this dopamine system is overactive and responsible for the positive symptoms of schizophrenia; whereas
A: LIMBIC
Q: #134 the meso-[] portion of this dopamine system is underactive and responsible for the negative symptoms
A: CORTICAL
Q: #136 WARNING: "Although Weinberg's scheme is still untested..." "It is not known how a loss of dopaminergic terminals in the prefrontal cortex leads to [] activity in the mesolimbic pathway.."
A: increased
Q: #137 The Dopamine Theory of Schizophrenia states that psychoses is the result of overactive or too much dopamine. Based on the action of successful antipsychotis and on the "Amphetamine Psychosis" effect of [] amphetamine
A: chronic
Q: #138 @Dopamine Receptor Types@ There have been six dopamine receptor sub-types that have been characterized in the brain: D1, D2a, D2b, D3, D4, and D5. Both of the [] receptors are the principle site of action for the phenothiazines and the butyrophenones.
A: D2
Q: #139 @Dopamine Receptor Types- D2@ THe D2 receptors are found in the cerebral cortex, in this [] structures (amygdala, nuc, accumbens, hippocampus) involved with emotionm, and in the striatum which is involved with motor behavior.
A: limbic
Q: #140 The D2a is on the postsynaptic surface and the D2b and the D3 are the inhibitory auto-receptors that are on the []-synaptic terminal.
A; pre
Q: #144 @Dopamine Receptor Types - D3s and D4s@ The D3,and D4 receptors are also found in limbic areas and in the cerebral cortex but not in [] areas like the striatum.
A: motor
Q: #145 [], one of the newer antipsychotic medications, blocks the D3, and D4 receptors best and only weakly blocks the D2's receptor types. ([] also binds to serotonin receptors and to histamine receptors.)
A: clozapine
Q: #146 @Molecular Mechanisms for D2 blcokade and clinical relief@ The molecular response to traditional antipsychotics is an intial INCREASED dopamine firing. Followed by a drastic [] in firing dopamine firing
A: DECREASE
Q: #147 This is due to a) enhancing [] synthesis by blocking the inhibitory autoreceptor which results in enhanced dopamine release; and b) the circuitry of the dopamine systems involved
A: dopamine
Q: #154 This increased sustained firing of dopamine neurons will induce a shut-down of the [] ("depolarization blockade")
A: cell
Q: #155 @Adverse Behavioral Effects@ The incidence of some motor disturbance induced by the medication has been reported as high as [] of all people receiving this medication
A: 90%
Q: #156 1.Acute Dystonia or Dystonic Reactions. Dystonia is a syndrome of sustained [] contractions. 2.Akathesia. Akathesia refers to a compulsion to move
A: muscle
Q: #157 3. Parkinson Syndrome or Parkinsonims (indistinguishable from clinical Parkinson's , bradykinesia, rigidity and tremor at []
A: rest
Q: #158 4. Tardive []. As the name implies, this is a late-onset motor disorder which occurs after a relatively long time on antipsychotic medication
A: Dyskinesia
Q: #159 @Adverse Behavioral Effects Tardive Tourette's Syndrome@ Tourette's is a nauro-motor disorder with onset during childhood and characterized by multiple chronic [] and vocal tics. Corpolalia (involunary utterance of vulagarity), echolalia, echopraxia (involunatry imitation of a movment)O
A: motor
Q: #160 One model is that it is the result of an imbalance between hyperactive nigral dopamine and underactive striatal acetylcholine. Chlopromazine and other meds can induce Tardive Tourete Syndrome, yet haloperidol has been considrere an effective treatment. Prevalence is [].
A: low
Q: #161 @Sobering Thoughts@ The ability to successfully treat schizophrenia with dopamine receptor blcokers does not neccessarily mean that schizophrenia is a [] disorder
A: dopamine
Q: #162 The strongest data comes from the treatment for Parkinson's disease. THe known causal pathology of Parkinson's is a loss of [] neurons in the Substantia Nigra. However, there is a []/Acetylcholine balance in the Basal Ganglia.
A: dopamine
Q: #165 In a sense there is too much [] for the pathalogically lowered dopamine. [] inhibitors (i.e. bringing down [] activity) can provide considerable relief from Parkinson's symptoms.
A: ACh
Q: #166 Therefore, in this case wehre blocking ACh provides relief one might to say that Parkinson's Disease is an [] disorder
A: ACh
Q: #167 The fact that we can provide relief of schizophrenic sx's by blcoking dopamine receptors just means taht schizophrenia can be treated through dopamine even though dopamine may not be the [] pathology
A: CAUSAL
Q: #168 @Dopamine Theory of Psychoses Challenged@ Clozapine blocks the specific serotonin receptor types 5HT2 and 5HT1c. Clozapine also blocks [] acetylcholine receptors
A: muscarinic
Q: #169 There are new medications that primarily block serotonin receptors and yet provide clinical relief to []. Two of these drugs are: Olanzapine (Zyprexa); and Risperidone (Risperdal)
A: psychoses
Q: #170 The actions of these new drugs (and the ability to better describe the actions of the "typical") have forced a more realistic accounting for more than just dopamine and [] in these models.
A: serotonin
Q: #171 A review of the newwest drugs shows some complex actions and the challenge to fins what presicely is the causal actions of the []
A: drug
Somatosensory and
Pain
A: behavior
Q: #003 The somatosensory system is unique from other sensory systems in two ways: 1) the receptor organ is the [], which means that it is the most far reaching sensory organ in the body; and 2) the sensations which are produced are quite varied.
A: skin
Q: #004 There are four distinct somatic (skin or body) sensations : 1) touch (fine touch) 2) proprioceptive sensations 3) [] 4) temperature (thermal sensations)
A: pain
Q: #005 @Receptor Types@ Each of the sensations are mediated by different receptor types which all have their somas in the [] root ganglion of the spinal cord.
A: dorsal
Q: #006 Pain receptors, called �nociceptors� have 3 sub-types 1) mechanical 2) thermal, >45o C 3) [], combination of 1 &2 and chemical all have bare nerve endings
A: polymodal
Q: #007 Touch receptors have 2 sub-types - those that are slow and those that are rapidly []; in addition skin with hair has different receptors.
A: adapting
Q: #008 These receptor types are different : 1) morphology of the peripheral ending 2) sensitivity to stimulus energy 3) diameter of the axon 4) whether the axon has [] or not
A: myelin
Q: #010 diameter of the axon: 0.2 -1.5 um - C fibers for slow burning pain 1 - 5 um - A-[] fibers for sharp pain 6-12 um - A-beta fibers for subcutaneous mechanoreceptors
A: delta
Q: #011 @Introduction@ There are three CNS pathways for somatosensory : 1) Anterolateral system 2) [] Column Medial Lemniscal system 3) Spino-Cerebellar tract
A: Dorsal
Q: #017 @Dorsal Column -Medial Lemniscal system@ I. the spinal cord Basically, the neurons in the spinal cord are located in the �butterfly� shape center of gray mater and the fibers of passage are located around these cell bodies in the [] mater.
A: white
Q: #018 The gray mater can be divided into the dorsal horn, the intermediate zone and the ventral horn OR it can be divided into [] layers.
A: 10
Q: #021 Layers I - V are in the dorsal horn layers VI and VII are in the intermediate zone layers VIII and IX are in the [] horn layer X is the area around the central canal.
A: ventral
Q: #023 There are six notable nuclei in the gray mater: 1) posterior marginal nuc. - (layer I) 2) substantia gelatinosa -(layers II and some III) 3) nucleus [] - (layers III,IV,V,and VI)
A: proprius
Q: #024 4) Clarke�s nucleus - (layer VII) but only in T1 through L2 5) intermediolateral nuc. - (layer VII) but only in T and upper L 6) [] nuclei -(layer IX)
A: motor
Q: #026 The white mater can be divided into : 1) the dorsal columns; 2) the [] columns; and 3) the ventral columns
A: lateral
Q: #028 Each segment of the cord has nerves entering and leaving called �roots�. There is a dorsal and a ventral root. There is a swelling of the dorsal root which is the collection of the cell bodies for the sensory neurons called the dorsal root [].
A: ganglion
Q: #031 Let us follow the Dorsal Column [] Lemniscal system form the receptor to the cerebral cortex. The pathway can be divided into the various processing steps which occur along the way (namely - how the information is passed on).
A: Medial
Q: #032 The receptor cells with their somas in the dorsal root ganglia are the [] Order neurons. These cells start the process.When these axons enter the spinal cord (the CNS) they take one of three courses.
A: 1st
Q: #033 Note: 1) receptors with [] diameter axons enter more medially; 2) fiber pathways typically are topographic
A: larger
Q: #034 1) they enter the Dorsal Column and ascend to more rostral CNS areas; 2) they send collaterals to and synapse in the dorsal horn; 3) they send collaterals to and synapse in the [] horn (for intrasegmental reflexes)
A: ventral
Q: #035 Fibers that enter the dorsal column do so in a topographical manner. the fibers from the more caudal areas of the body occupy the most medial portions of the [] column.
A: dorsal
Q: #039 By the time these fibers reach the upper cord there are two distinct swellings or bumps in the dorsal column. The medial bumps are called the fasciculus gracilis and the more [] bumps are called the fasciculus cuneatus.
A: lateral
Q: #040 The most medial information in fasc. gracilis conveys somatosensory information from the lower limbs, and more lateral on fasc. gracilis concerns input from [] trunk (sacral, lumbar and thoracic cord);
A: lower
Q: #041 The most medial information in fasc. cuneatus conveys somatosensory information from the upper limbs, and more lateral on fasc. cuneatus concerns input from neck and [] trunk (upper thoracic and cervical cord).
A: upper
Q: #043 These fibers will synapse in the medulla in a set of four nuclei called the dorsal column nuclei; the two most medial of these are called the nuclei gracilis and the lateral nuclei are the nuclei [].
A: cuneatus
Q: #044 The neurons of the dorsal column nuclei constitute the 2nd Order Neurons. The axons from these neurons will then cross the midline as the Internal Arcuate Fibers and then proceed rostrally as the Medial [].
A: Lemniscus
Q: #045 The Medial Lemniscus synapses in the [], specifically onto the ventral posterior lateral nucleus of the [] (VPL) and onto the Posterior nuclei (P). The neurons of VPL and P constitute the 3rd Order neurons of this system.
A: Thalamus
Q: #046 @The Nuclei of the Thalamus@ The Thalamic nuclei can be grouped into 4 categories: 1) the anterior group; 2) the medial group; 3) the ventral group; and 4) the [] group
A: posterior
Q: #048 The [] group receives input from the hypothalamus and the hippocampus and send out projections to the cingulate and frontal cortex. It may be involved in memory and emotion behaviors.
A: Anterior
Q: #049 The Medial group is also implicated in memory. The Ventral group has a portion that is involved in motor control and another portion that is involved in somatosensory input to [].
A: cortex
Q: #050 The Posterior group has a portion involved in visual and auditory input to cortex, and another large portion (the Pulvinar) that has extensive cortical connections that are involved in higher [] processing.
A: visual
Q: #051 @Dorsal Column - Medial Lemniscal system@ The neurons of VPL and P project in a portion of the Internal Capsule to the cerebral cortex, specifically the [] Somatosensory Cortex or SI ( the postcentral gyrus, corresponding to areas 3a, 3b, 1, 2 using Brodmann�s numbers).
A: Primary
Q: #056 The processing does not stop at this synapse in the cerebral cortex, these [] areas have important projections. let us first examine the layers of cerebral cortex.
A: cortical
Q: #057 The cerebral cortex has six individual cellular layers referred to as Layers I through VI. Cortical layers II, III, V, and VI have the neurons whose axons project out of the cortical mantle. Cortical layer [] is the input layer of the cerebral cortex.
A: IV
Q: #058 There are three general types of cerebral cortical projections : 1. []- cerebral cortex will project to the neighboring cortical areas that are next to a given area;
A: associational
Q: #060 2. [](or commissural) - cortical areas will project to the mirror area in the other hemisphere via the Corpus Callosum;
A: callosal
Q: #061 3. �Projection� connections - cortical neurons will project outside the cortex to sub-cortical areas throughout the CNS from [] structures all the way down to the spinal cord.
A: telencephalic
Q: #063 Specifically, the projections from the Primary Somatosensory Cortex are : Layers II and III - makes associational connections to [] and associational cortices;
A: motor
Q: #064 Layer V - projects to the dorsal column nuclei, as well as to the dorsal horn of the spinal cord ; and to the striatum and brain stem in general; Layer VI - projects to the VPL and P groups of the [].
A: Thalamus
Q: #066 The projections from the Secondary Somatosensory Cortex (SII) are curious. Although SII is approximately [] the size of SI, it is higher order somatosensory processing.
A: 1/4
Q: #067 SII is the first cortical processing in which both sides of the body are represented. Over [] of SII neurons are affected by attentional state (in both directions).
A: 80%
Q: #068 SII receives from all 4 areas of SI and projects to the Insula which then projects to amygdala and hippocampus. SII is the relay of somatosensory information into the [] system.
A: Limbic
Q: #072 @Antero-lateral system - Pain@ Nociception refers to the reception of signals in the [] evoked by the activation of certain receptors specialized for tissue damage information. Pain is the perception of an aversive sensation that originates from a specific area of the body.
A: CNS
Q: #073 Nociceptors can be sensitized by chemicals released during tissue damage which all act to either decrease the threshold of nociceptors or to [] activate certain nociceptors.
A: directly
Q: #074 Chemicals that perform this function include : [], ATP, ACh, 5HT, Prostaglandin E2, bradykinin, and Substance P.
A: histamine
Q: #076 Pain can be due to injury of peripheral nerves or a loss of the peripheral nerves (i.e. phantom limb pain). Pain may also be due to CNS damage in the ventrobasal [] (the thalamic syndrome).
A: thalamus
Q: #077 The concept of a 1st, 2nd, 3rd Order neuronal sequence is difficult with pain. Certainly the nociceptor is the [] Order neuron in this system.
A: 1st
Q: #078 The receptors for nociception and pain are the A-[] and C fibers. Both release two neurotransmitters: glutamate which is excitatory, and a variety of peptides, in particular substance P, which is also excitatory.
A: delta
Q: #079 The A-delta and C fibers immediately bifurcate/ spilt when they enter the cord and ascend and descend for a few segments in the []�s tract and then actually enter the gray mater.
A: Lissauer
Q: #080 The 2nd Order neurons are in the dorsal horn and there are two classes: 1) the neurons in Lamina I (posterior marginal nuc.) 2) the neurons in Lamina []-VIII (nuc. proprius)
A: V
Q: #082 [] I (posterior marginal nuc.) has two types of neurons : nociceptive specific - which respond only to A-delta and C fibers; and wide dynamic range - which respond also to mechano-receptors.
A: Lamina
Q: #083 Lamina V-[] (nuc. proprius) has wide dynamic range - which respond also to mechanoreceptors.
A: VIII
Q: #084 �[] pain� is the perception of pain from the viscera felt as cutaneous pain. The cause may be the divergence of cutaneous and visceral input onto the same projection neurons in the cord.
A: Referred
Q: #085 The fibers of the 2nd Order neurons in the cord immediately cross (not all, but most) and travel in the ventral-lateral portion of the [] mater, referred to as the Antero-Lateral section.
A: white
Q: #087 There are at least seven general targets of the 2nd Order neurons, which constitute the 3rd Order neurons. However, it is more useful to consider these 3rd Order neurons as individual sub-systems of the [] system.
A: Anterolateral
Q: #088 1. Spino-thalamic tract. Originates from Lamina I and V-VII; 2. Spino-reticular tract. Originates from Lamina [] (and VIII) and has some of its fibers remain ipsilateral in the anterolateral portion of the cord;
A: VII
Q: #089 3. Spino-mesenceaphalic tract. Originates in Lamina I and []; 4. Spino-cervical tract. Originates in Lamina III and IV from neurons that also respond to tactile stimulation and ascend in the �dorso-lateral� portion of the cord;
A: V
Q: #090 5. some Lamina III and IV ascend in the [] columns and project to the [] column nuclei; 6. Spino-hypothalamic tract. 7. Spino-ponto-amygdalo tract.
A: dorsal
Q: #091 There are two principle thalamic targets for the anterolateral systems : 1. the medial group - intralamina nuclei, and the central nucleus; 2. the lateral group - ventrobasal nuclei (which includes VPL) and the [] group.
A: posterior
Q: #092 the [] group - receives input from lamina VII and VIII; the lateral group - receives input from lamina I and V.
A: medial
Q: #093 The cortical targets : [] group projects diffusely to ipsilateral cortex; lateral group projects the primary somatosensory cortex; other cortical targets include SI, SII, cingulate gyrus, prefrontal cx
A: medial
Q: #096 There are two other cerebral cortical areas that have been involved in pain processing: the cingulate cortex and the [].
A: insula
Q: #101 The Insula seems to be involved with [] the sensory, affective (emotional), and cognitive aspects of the pain response.
A: integrating
Q: #102 The �[] Theory� of pain by Melzack and Wall. States that the firing of neurons in the cord responsible for pain is a balance between the nociceptive input and the activity of non-pain input to the cord.
A: Gate
Q: #105 Central Gray Analgesia. When the central gray nucleus of the []-encephalon is electrically stimulated the animal is rendered analgesic, without loose of other tactile sensations. Other areas include ventrobasal thalamus, internal capsule.
A: mes
Q: #106 There is control of pain from rostral areas of the CNS that descend to the cord. Lesions of the dorsolateral [] suppresses stimulus induced analgesia.
A: funiculus
Q: #107 Descending control of pain system: 1. the prefrontal cerebral cortex projects to the central gray region of the mesencephalon; 2. the central gray projects to the raphe magnus and the nuc. reticularis gigantocellularis in the [];
A: medulla
Q: #108 3. these medullary nuclei make inhibitory contact in lamina I,II, and [] in the dorsal horn of the cord.
A: V
Q: #109 3. these medullary nuclei make inhibitory contact in lamina I,II, and V in the dorsal horn of the cord. Central [] and the rostroventral medulla are sensitive to morphine.
A: gray
Q: #111 @Acupuncture@ Acupuncture resulted in activation of the [] and nucleus accumbens and deactivation of the rostral part of the anterior cingulate cortex, amygdala formation, and hippocampal complex; control stimulations did not result in such activations and deactivations.
A: hypothalamus
Q: #113 Acupuncture activates structures of descending anti-nociceptive pathway and deactivates multiple [] areas subserving pain association.
A: limbic
Q: #114 There are three classes of endogenous opiates : 1) pro-enkephalins 2) pro-opio-melano-cortins (POMC) 3) pro-[]
A: dynorphin
Q: #117 Classes of endogenous opiates : 1) pro-enkephalins (met- and leuenkephalins) 2) pro-opio-melano-[] (POMC) (beta-endorphin) 3) pro-dynorphin (dynorphin and alphaneoendorphin)
A: cortins
Q: #118 All five are analgesic. [] and dynorphin are in central gray and in the rostroventral medulla and in the dorsal horn of the cord; whereas endorphin is only in hypothalamic neurons that project to central gray and the brain stem.
A: Enkephalins
Q: #119 @Endorphin Pathways@ The neurons that use endorphins are restricted to the hypothalamus. These specific hypothalamic neurons project to a variety of limbic structures like the central gray, septal area, amygdala, locus coeruleus, and nucleus [].
A: accumbens
Q: #120 @Enkephalin Pathways@ Enkephalins are present almost everywhere in the CNS. Like GABA, enkephalins are used by [] in local circuits. There are no projection neurons (i.e. Golgi Type I) that use enkephalins.
A: interneurons
Q: #122 @Opiate Receptors@ The following are the 5 different subclasses of opiate receptors : a) the mu (m) - m1 and m2 receptors b) the sigma (s) - the PCP/s receptor and the s PCP insensitive receptor c) the [] (k) receptor
A: kappa
Q: #123 d) the delta (d) receptor e) the [] (e) receptor All these receptors are involved in one way or another in the mediation of analgesia . The mu receptor in particular plays a critical role in mediating analgesia
A: epsilon
Q: #124 the respiratory depression so distinctive of opiate use is mediated by mu, sigma and delta receptors, but not by the [] receptor
A: kappa
Q: #125 The gastrointestinal effects of the opiates seem to be mediated a combination of [] receptor activity at the brain level and by [] and kappa receptors in the intestines
A: mu
Q: #126 The enkephalins have a high affinity for the [] receptor and some affinity for the mu receptor, but no affinity for the kappa receptor.
A: delta
Q: #127 [] has an extremely high affinity for the kappa receptor and a low but significant affinity for mu and delta receptor types .
A: Dynorphin
Q: #128 Directly applying 5HT or NE in the cord will produce analgesia. The rostroventral medullary nuclei use 5HT as a transmitter and maybe pontine and other medullary neurons use [].
A: NE
Q: #131 @Antero-lateral system - Pain@ [] activates these descending systems by suppressing the activity of inhibitory (GABA) interneurons that normally inhibit the descending systems.
A: Morphine
Q: #132 At the level of the cord: there are [] inhibitory interneurons at the primary sensory neuron synapse to the projection neuron. Descending 5HT and NE neurons synapse on both the interneurons and the projection neurons.
A: enkephalin
Q: #133 There are [] receptors on both sides of the at the primary sensory neuron synapse to the projection neuron; and so morphine exerts two effects one pre-synaptic and one postsynaptic in controlling pain.
A: mu
Q: #136 Pre-synaptically - morphine will inhibit the release of the neurotransmitter (by decreasing [] influx); Post-synaptically - morphine hyperpolarizes the postsynaptic surface.
A: Ca++
emotional behavior
A: emotional
Q: #002 In general, in motivation of what �Limbic System� areas play a critical role ?
A: behavior
Q: #003 Down to what caudal -cephalon structure from the tel-encephalon the collection of Limbic structures has grown to include ?
A: metencephalon
Q: #004 Only what -cephalon strucutre has no significant limbic structure ?
A: Myelencephalon (the medulla)
Q: #005 What 6 (3 gyruses and 3 cortexes) Tel-encephalic limbic areas are in the cerebral cortex ?
A: 1) cingulate gyrus 2) para-hippocampal gyrus 3) sub-callosal gyrus 4) entorhinal cortex 5) prefrontal cortex 6) temporal cortex
Q: #006 What are 4 Sub-cortical tel-encephalic limbic areas :
A: 1) hippocampal formation 2) amygdala 3) septal nuclei 4) nuc. accumbens
Q: #007 What are 3 di-encephalic limbic areas :
A: 1) hypothalamus 2) anterior thalamus 3) the habenula
Q: #008 What are 3 mes-encephalic limbic areas :
A: 1) interpeduncular nuc. 2) central gray 3) raphe nuc
Q: #009 What is 1 met-encephalic limbic areas :
A: 1) locus coeruleus (A6)
Q: #010 What kind of connections all limbic areas have ?
A: intensely reciprocal
Q: #011 Intensely reciprocal connection of limbic areas when project to one another and form a network what kind of loops do they form:
A: closed
Q: #012 What circuit propesed in the 1930�s illustrates loops connections of limbic areas ?
A: Papez
Q: #013 What two principle limbic structures we will examine this week (along with associated cerebral cortical areas that are connected to these structures) ?
A: 1) the hypothalamus 2) the amygdala
Q: #014 @Hypothelamus@ What is the most important component of the limbic system ?
A: hypothalamus
Q: #015 What 8 behaviors an animal generate hypothalamus structure plays critical role ?
A: virtually every behavior: 1) eating 2) drinking 3) arousal 4) learning 5) aggression 6) sleep 7) sex 8) temperature regulation
Q: #016 What are four essential roles of hypothalamus ?
A: 1) monitoring of body functioning (for example blood glucose, insulin, oxygen, CO2, and a variety of peptides released in the GI tract during digestion) 2) maintain a state of homeostasis 3) maintains the animal�s hormonal environment 4) trigger a Sympathetic response
Q: #017 By interactions with what structure hypothalamus maintains the animal's hormonal environemnt ?
A: pituitary
Q: #018 Where is Hypothalamus in the brain stem ?
A: just below (ventral) to the thalamus
Q: #019 What is the hypothalamus bordered by from the ventral surface rostrally ?
A: optic chiasm
Q: #020 What is the hypothalamus bordered by from the ventral surface laterally ?
A: cerebral peduncles
Q: #021 What is the hypothalamus ends in ?
A: the Mammillary bodies
Q: #022 In what 2 general areas from a ventral aspect, the hypothalamus can be divided into ?
A: 1) lateral area 3) medial areas
Q: #023 What has medial area most of the hypothalamus ?
A: nuclei
Q: #024 What has lateral area most of the hypothalamus ?
A: fibers
Q: #025 The nuclei of the medial area we will examine, in how many sub-groups can be divided on a rostral to caudal scheme ?
A: 4
Q: #026 What are the 4 divisions of the medial area nuclei ?
A: 1. the pre-optic area 2. the supra-optic area 3. the tuberal area 4. the mammillary bodies
Q: #027 @Hypothalamus - Pre-optic@ What are the 2 nuclei of the pre-optic area ?
A: 1. medial preoptic nuc. 2. lateral preoptic nuc.
Q: #028 What kind of receptors lateral preoptic nuc has ?
A: osmoreceptors
Q: #029 Sexually, what kind of nucleus preoptic nucleus is ?
A: dimorphic nucleus (branching and number of spines is greater in females)
Q: #030 What nucleus preoptic nucleusis sensitive to at critical times ?
A: endrogens ( and it may be involved in mediating estrous)
Q: #031 How is the volume of the sexually dimorphic nucleus of the preoptic.area (SDN-POA) of the rat varies among sexes ?
A: It is several times larger in males than in females
Q: #032 What kind of sexual behavior medial preoptic nuc. mediates ?
A: masculine
Q: #033 What kind of sexual behavior Ventromedial Hypothalamus (VMH) mediates ?
A: femenine
Q: #034 Was any difference in either volume or cell number of SDN cells was observed between homosexual and heterosexual men ?
A: No
Q: #035 @Hypothalamus - Supraoptic@ What are the 5 nuclei of the supraoptic area ?
A: 1) anterior hypothalamus 2) suprachiasmatic nuc. 3) supraoptic nuc. 4) paraventricular nuc 5) OVLT (organum vasculorum lamina terminalis)
Q: #036 What the anterior hypothalamus is involved in ?
A: thermoregulation (specifically heat dissipation)
Q: #037 What nucleus also plays role in thermoregulation (especially in generating fever) ?
A: preoptic nuc.
Q: #038 What nuc. receives direct projections from the retina, and seems to be involved with the mediation of biological rhythms Seasonal Affective Disorder Syndrome ?
A: The suprachiasmatic nuc.
Q: #039 What Morphometric analysis of the human hypothalamus revealed about Interstial nuclei -3 (INAH-3)
A: It is smaller in homosexual men (who died from AIDS) than heterosexuals. (The INAH-3 was also found to be smaller in homosexual men compared to heterosexual men and that the homosexual INAH-3 was similar in size to heterosexual women.)
Q: #040 To what structure both Supraoptic nuc. cells and the Paraventricular nuc. cells project to ?
A: the posterior pituitary.
Q: #041 What are the two types of cells in Supraoptic nuc. cells
A: 1) magnocellular 2) parvocellular
Q: #042 What kind of Supraoptic nuc. cells that send their axons into the posterior pituitary ?
A: magnocellular [neurons]
Q: #043 What kind of hormones mangocelllar cells make ?
A: oxytocin and vasopressin (AVP, also known as ADH - antidiuretic hormone)
Q: #044 Where does OVLT sits ?
A: the rostral base of the 3rd ventricle
Q: #045 What does OVLT contains ?
A: osmoreceptors
Q: #046 What does OVLT osmoreceptor's play role in ?
A: thirst and fluid balance.
Q: #047 @ Hypothalamus - Tuberal Area@ What are the 4 nuclei of the tuberal group ?
A: 1) ventromedial hypothalamus (VMH) 2) the dorsomedial hypothalamus (DMH) 3) the arcuate nuc. 4) the periventricular nuc.
Q: #048 How is the stalk that connects the pituitary called ?
A: the infundibulum
Q: #049 How is the point of connection of the pituitary called ?
A: median eminence
Q: #050 What does the VMH is involved in ?
A: food regulation, once considered to be the �satiety� center of the brain because lesions of this area led to frank obesity
Q: #051 What is The 3rd Ventricle ?
A: a midline ventricle of the diencephalon and it bisects the hypothalamus as well as he thalamus.
Q: #052 What are The nuclei immediately surround this ventricle ?
A: the periventricular nuc. and is in this tuberal area
Q: #053 @Hypothalamus - Mammillary Body Area@ What are 2 mammillary body are nuclei ?
A: 1) the Posterior nuc. and the 2) mammillary bodies
Q: #054 Where does mamillary bodie pair of nuclei involved in (3 function) ?
A: thermoregulation (heat conservation) 2) autonomic functioning 3) memory consolidation
Q: #055 @ Hypothalamus - and the Pituitary@ WHat are the two parts of The pituitary ?
A: 1) the anterior pituitary or the adenohypophysis; and 2) the posterior pituitary or the neurohypophysis.
Q: #056 How many ways hypothalamus interacts with the two parts of the pituitary ?
A: TWo
Q: #057 @I. the posterior pituitary.@ Which two hypothalamic nuclei send their axons into the pituitary where these axon terminals will end such that they will release their vesicle contents into the general circulation.
A: the paraventricular and the supraoptic
Q: #058 What are the 2 hormones that are made in the hypothalamus and released from the posterior pituitary are: (Thus, the posterior pituitary is nothing more the place these axons end.)
A: 1) oxytocin 2) vasopressin (AVP, also known as ADH - antidiuretic hormone)
Q: #059 In what tonic patter magnocellular neurons that release oxytocin fire
A: a phasic pattern
Q: #060 In what patern the neurons that release vasopressin fire ?
A: a tonic pattern
Q: #061 @II. the anterior pituitary.@ Through which medium The parvocellular neuron of the paraventricular and supraoptic nuclei as well as other nuclei in the hypothalamus interact with the anterior pituitary ?
A: the blood (using a specialized portal system)
Q: #062 Where are parvo cellular cells located ?
A: 1) in the tuberal nuceli (in particular the the arcuate, and the peri-ventricular); 2) the paraventricular nuc (80% of these cells are parvocellular and 20% are magnocellular), and 3) the preoptic nuc; and 4) the suprachiasmatic nuc.
Q: #063 What does the agent released by the hypothalamic neurons from their terminals into a portal system ?
A: irrigates the anterior pituitary cells.
Q: #064 What does the agents' "releasing factors", released by hypothalamic neurons ?
A: provoke the anterior pituitary cells to secrete their hormones into the general circulation
Q: #065 What factor there is for every hormone released by the anterior pituitary ?
A: hypothalamic factor (that promotes its release or inhibits its release as in the case if �inhibiting factors�.)
Q: #066 By interacting with the pituitary in addition to the more common neural connections, the hypothalamus can exhibit how many types of CNS processing ?
A: four
Q: #067 @ Hypothalamic Processing- Neural In/Endocrine Out@ What is an ecample of this type of hypothalamic reflex ?
A: Milk ejection or �let down� (Somatosensory input from a nursing infant is conveyed by the usual pathways and results in the release of oxytocin which travels via the blood to the breast. As learning occurs, the mere sound of an infant crying will cause the hypothalamus to release oxytocin.
Q: #068 @ Hypothalamic Processing- Neural In/Neural Out@ What is neural input leading to the neural output for the necessary motor behavior of defense/aggression ?
A: The mediation of aggressive/defensive behavior
Q: #068 What is a critical loop for agression ?
A: The mutual innervation between the hypothalamus and the amygdala ( These two nuclei have intense reciprocal connections)
Q: #069 @Hypothalamic Processing- Endocrine In/Neural Out@ What is an example of is type of processing ?
A: Sexual behavior ( In males, androgens act on the neurons of the medial preoptic to mediate copulation. In females, estradiol and progesterone act on the neurons of the VMH to mediate lordosis)
Q: #070 What does the Estradiol pretreatment appears to cause an increase in ?
A: the number of progesterone receptors in the hypothalamus (and the subsequent injection of progesterone will cause an increase in the number of oxytocin receptors in VMH)
Q: #071 What are 3 other CNS areas involved in sexual behavior ?
A: both rostral (cerebral cortical especially the 1) temporal lobe, and 2) the amygdala), and caudal (3) central gray) to the hypothalamus.
Q: #072 @Hypothalamic Processing- Endocrine In/Endocrine Out@ What is an example of this processing ?
A: urine output (Blood borne agents like angiotensin II which marks low blood volume, will be detected by hypothalamic neurons that will in turn cause other hypothalamic neurons, specifically the paraventricular and supraoptic nuc., to release vassopressin in order to retain more water)
Q: #073 Perhaps a better example are the many feedback loops of circulating hormones that will be detected by hypothalamic neurons which in turn result in a change in the release of hypothalamic releasing factors into the [] pituitary.
A: anterior
Q: #074 @Hypothalamus the Lateral Area@ What are the 3 primary fibers from lateral area ?
A: 1) the medial forebrain bundle 2) the nigro-striatal pathway 3) other fibers of passage
Q: #075 What was once considered the �hunger center�because lesions in this area produced profound aphagia - lack of eating.
A: The lateral hypothalamus (LH)
Q: #076 What the LH also supports ?
A: self-stimulation (due to the fibers of the MFB)
Q: #077 @Hypothalamus Neural Afferents@ What are 9 nerural Neural afferents (inputs) ?
A: 1. amygdala via stria terminalis 2. hippocampus via the fornix 3. basal ganglia 4. thalamus 5. septal nuclei 6. central gray 7. the reticular formation 8. retina 9. all the nuclei that contribute to the medial forebrain bundle like locus coeruleus, raphe, DA cells
Q: #078 @Hypothalamus Neural Efferents@ What are 9 Neural efferents (outputs) ?
A: 1. amygdala 2. thalamus (anterior thalamus) 3. interpeduncular nuc. 4. septal nuclei 5. reticular formation 6. the locus coeruleus 7. nuc. of the solitary tract (NTS) 8. dorsal motor nucleus of the vagus 9. intermediolateral area of the cord 10. central gray 11. nuc. accumbens
Q: #079 What the paraventricular nuc in particular sends to ?
A: 6. the locus coeruleus 7. nuc. of the solitary tract (NTS) 8. dorsal motor nucleus of the vagus 9. intermediolateral area of the cord
Q: #080 What is the arcuate nuc in particular sends to ?
A: 10. central gray 11. nuc. accumbens
Q: #081 @ Hypothalamus - The Autonomic Nervous System@ To what nuclei in the brain stem and the spinal cord the hypothalamus projects to ?
A: those that will act on the cells of the intermediolateral nucleus
Q: #082 @Limbi system an behavior@ The readings divides the issues as 1) Motivation and Addiction a) temperature b) feeding c) drinking d) reinforcement 2) Emotional States and Feeling a) [] b) cerebral cortical involvement
a: amygdala
Q: #083 How is The term �motivation� is defined ?
A: neuronal and physiological factors that initiate, sustain and direct behavior (This is fueled by �drive states�. And a servo-control system is the model.
Q: #084 @Hypothalamus Temperature Regulation@ What are the two basic inputs:
A: 1) peripheral temperature (which is picked up by receptors on the skin) 2) central receptors to pick up body temperature
Q: #085 What two structures are involved in regulating temperature;
A: The anterior and posterior hypothalamus
Q: #086 What is located only in the anterior hypothalamus ?
A: actual temperature detectors (i.e. blood temperature)
Q: #087 What results from Stimulating the anterior hypothalamus ?
A: peripheral vasodilation and suppression of shivering with the overall drop in body temperature.
Q: #088 What results from stimulating the posterior hypothalamus ?
A: the opposite effect
Q: #089 @ Hypothalamus Feeding Behavior@ What is the key CNS structure in One of the most critical behaviors that we have is feeding. It is an incredibly complex process that involves different types of nutrients and different metabolic needs of the system ?
A: The hypothalamus
Q: #090 Is true that our body weight is rather well controlled and the mechanisms for control (�set points�) are probably many .
A: Yes (One of the interesting models in the readings is one of energy expenditure relative to our body weight.)
Q: #091 Early findings have implicated the hypothalamus in feeding regulation: 1. (1942) lesions of the [] would result in animals that would overeat to obesity, whereas stimulation of [] would suppress eating.
A: ventromedial hypothalamus (VMH)
Q: #092 2. (1951-54) lesions of the [] caused animals to stop eating and drinking; whereas stimulation of [] would result in animals eating and drinking.
A: lateral hypothalamus (LH)
Q: #093 @Hypothalamus Feeding - VMH Lesions@ Since these initial studies, it has been found that VMH lesioned animals are finicky and if given the choice will specifically overeat [].
A: carbohydrates
Q: #094 What is a key hormone affecting caloric homeostasis and is influenced by many factors ?
A: Insulin
Q: #095 What does lesions of the VMH also disrupts ?
A: the connections of the paraventricular nuc. to the �vagal complex� (i.e. nucleus of the solitary tract, dorsal motor nuc. of the vagus, etc.). The increased insulin release following VMH lesions may be the result of disrupting this pathway.
Q: #096 What are the 4 effects on eating behavior of specific neuro-transmitters when injected directly into the paraventricular nuc. that has been described ?
A: 1. norepinephrine (NE) stimulates the intake of carbohydrates; 2. serotonin (5HT) inhibits carbohydrate intake; 3. galanin stimulates the intake of fats 4. opiates stimulates protein intake Hypothalamus
Q: #097 With what neurotransmiter, Galanin, a neuroactive peptide, coexists with ?
A: NE (so both are released from these neurons)
Q: #098 Secretion of what galanin and insuling alters ?
A: insulin and corticosterone (secretion indicating that it alters metabolism in a complex fashion)
Q: #099 What structure is the most effective site for eliciting feeding behavior ?
A: LH (Rats given NPY in the LH eat ravenously, will work hard for food, will eat adulterated food and eat though shocked !!)
Q: #100 While it may be a potent factor in feeding, [] has multiple effects: [] suppresses ovulation and inhibits sexual behavior.
A: NPY
Q: #101 In addition, many neurons in the [] are �glucose-sensitive� in that these neurons will change their firing rates in response to the levels of glucose in the blood supply through the brain.
A: LH
Q: #102 What 3 damage can result from Lesions to ventromedial and lateral hypothalamic areas ?
A: 1) altered sensory input; 2) altered set point; and 3) altered arousal levels.
Q: #103 Lesions of [] result in animals that are highly responsive to aversive and positive aspects of food (seen also in human obesity data).
A: VMH
Q: #104 @Hypothalamus - Feeding Long and Short term Cue@ What would shorter term cues include ?
A: taste features of food and the many hormonal signals of digestion (CCK is a prime example). (Both long and short term cues must work together to achieve regulation.)
Q: #105 @Feeding - Genetic Factors and Long term Cue@ What cell release leptin ?
A: fat cells (and Leptin serves as a long term hormonalcue of fat stores)
Q: #106 What deos Leptin does?
A: suppresses appetite and increases metabolic rates. (The absence of leptin leads to obesity)
Q: #107 What are three possible mechanisms in the leptin story ?
A: 1) the lack of leptin itself; 2) an abnormality of the leptin receptor and 3) abnormal responses to adequate leptin interacting with normal receptors.
Q: #108 @Hypothalamus � Circuits in Hunger@ How many populations of neurons in the LH that stimulate hunger and decrease metabolic rate ?
A: 2
Q: #109 What peptide nerotransmitters These neurons secrete ?
A: 1) peptide neurotransmitters 2) melanin-concentrating hormone (MCH) 3) orexin.
Q: #110 What do the Injections of MCH or orexin into the brain induces ?
A: eating
Q: #111 What does the food deprivation leads to ?
A: increased messenger RNA for both MCH and orexin.
Q: #112 @Hypothalamus � Circuits in Hunger@ Where are The axons of MCH or orexin neurons project to brain areas involved in ?
A: motivation (They also project to neurons that effect the autonomic nervous system)
Q: #113 How does gluco- and lipo-provation induce eating ?
A: via neurons that use neuropeptide Y (NPY)
Q: #114 What Infusions of NPY in the hypothalamus produces ?
A: ravenous eating.
Q: #115 What are the two sites of action for NPY ?
A: 1) One is in the LH where it produces eating by stimulating MCH and orexin neurons. 2) The other is the paraventricular nucleus where it produces metabolic effects like insulin secretion, Hypothalamus � Circuits in Hunger decreased breakdown of triglycerides in adipose tissue, and decreased body temperature.
Q: #116 What does Food deprivation do to the level of NPY ?
A: decreases
Q: #117 @Hypothalamus � Circuits in Hunger@ Where are The neurons that secrete NPY ?
A: in the arcuate nucleus in the hypothalamus
Q: #118 Where do the neurons that secrete NPY project (2 structure) ?
A: to both the paraventricular nucleus and to the MCH and orexin neurons in the LH.
Q: #119 What supressed eating and inhibits the production of NPY ?
A: Leptin
Q: #120 What are NPY neurons' leptin receptor sites do if activated ?
A: are inhibitory
Q: #121 What kind of system is in the arcuate nucleus ?
A: satiety system
Q: #122 What peptide do arcuate neurone secrete ?
A: CART (cocaine and amphetamine regulated transcript).
Q: #123 Injections of CART into the ventricles inhibits even [] feeding, and CART is absent in ob mice.
A: NPY
Q: #124 CART neurons send projections to the paraventricular nucleus and to the LH. CART neurons increase metabolic rate and inhibits MCH and orexin neurons in LH, and thereby suppress [].
A: eating
Q: #125 CART neurons also have leptin receptors, but this time these receptors stimulate the CART neurons so this may be the way that leptin stops [].
A: eating
Q: #126 Serotonin also has some role in eating behavior. There are serotonin receptors in the PVN that [] eating. Fenfluramine is a serotonergic agonist and has been used in the treatment of obesity because it will suppress appetite.
A: inhibit
Q: #127 The PVN projects to the NTS and the vagal complex. The [] seems to be especially involved in carbohydrate intake and the DMV mediates insulin release. (The NST also is the first nucleus to receive sensory information from the gut about digestion.)
A: NTS
Q: #128 @Hypothalamus � Circuits in Hunger Hypothalamus and Reinforcement@ The role of other factors besides ]states is critical. Hedonics especially - reinforcement.
A: drive
Q: #129 Wat mediates reinforcement ?
A: The medial forebrain bundle
Q: #130 All the monoamine nuclei feed into this system, but [] seems to be the key.
A: dopamine
Q: #131 What cells are importand dopamine sub-system ?
A: the cells of the Ventral Tegmental area
Q: #132 Where are cell of the ventral tegmental are projecting to ?
A: the nuc accumbens
Q: #133 note that there are many neurotransmitter systems that are involved in the VTA to Accumbens circuit. In addition, there are [] receptors in the nuc accumbens.
A: opiate
Q: #134 ALSO NOTE: Tolerance is NOT a feature of addiction. It is simply the decrease in a drug [] following repeated doses. It is not exclusively fixed to the euphoria of certain drugs.
A: effect
Q: #135 What two strucutre mediates Conscious feeling ?
A: 1) cingulate cortex 2) the frontal lobes
Q: #136 What two 3 brain structure mediates Emotional states ?
A: 1) amygdala 2) hypothalamus 3) other brain stem areas
Q: #137 Early studies (1930�s circa) showed that stimulation of the [] produces a sympathetic response similar to anger and/or aggression. In fact, different types of aggression could be elicited.
A: lateral hypothalamus (LH)
Q: #138 WHat stimulation produces predatory attack ?
A: LH
Q: #139 What stimulation produces �affective� attack (physical display of anger) ?
A: medial hypothalamus
Q: #140 What stimulation produces fearful flight/escape behavior ?
A: dorsal hypothalamus
Q: #141 All of the aggressive behaviors produced by hypothalamic stimulation seems to be the result of hypothalamic activation of what (3 strucutre) ?
A: more caudal areas (like the 1) central gray, 2) ventral tegmental area), or activation of the 3) amygdala.
Q: #142 @Amygdala@ Where does the amygdala sits ?
A: Below the cerebral cortex in the tip of the temporal lobe.
Q: #143 What are the amygdala's two main divisions ?
A: 1) corticomedial 2) basolateral
Q: #144 The amygdala may play a pivotal role between those areas that process the [] expression of emotion (hypothalamus) and those cortical areas that process feeling like fear (cingulate, parahippocampal gyrus and the prefrontal cortex.
A: somatic
Q: #145 What does inferotemporal cortex seems to mediate, as it related to reading of facial expression ?
A: specific facial memory
Q: #146 What does the amygdala seems to process , as it related to reading of facial expression?
A: the connection of emotional expressions
Q: #147 @Amygdala - Aggression@ In what two roles does amygdala plays ?
A: aggressive behavior and memory (a high density of estrogen and androgen receptors)
Q: #148 What lesions of the amygdala has been used to control ?
A: pathological aggression seen in certain cases of temporal lobe epilepsy
Q: #149 What role corticomedial amygdala appears to play
A: an inhibitory role in �predatory� aggression/ attack (predatory aggression is unemotional killing)
Q: #150 What two lesions facilitates predatory attack ?
A: 1) Lesions of the corticomedial area 2) lesions of the stria terminalis
Q: #151 Where does basolateral amygdala appears to play an excitatory role ?
A: �affective� aggression (affective aggression is a loud emotional display of aggressive postures) (stimulation of the basolateral area eads to affective aggression even if the stria terminalis is cut)
Q: #152 What lesions of the entire amygdala lead to ?
A: the �Kluver-Bucy Syndrome�
Q: #153 What 4 characteristics �Kluver-Bucy Syndrome�t has in primates ?
A: 1. over attentiveness, restlessness, responds to all stimuli 2. hyper-orality 3. psychic-blindness (visual agnosia) - indiscriminately approach anything even potentially harmful animals 4. hypersexuality - increased activity and a lack of discrimination of targets
Q: #154 To what kind of epilepsy The amygdala seems to be linked ?
A: �Temporal Lobe Epilepsy� (TLE)
Q: #155 To what lobe is TLE seizuredisorder related in the the cerebral cortex ?
A: Temporal lobe
Q: #156 What kind of behavior is associated Often with TLE ?
A: violent behavior
Q: #157 What is one of the models approaching treatment of TLE ?
A: The possibility of the seizure �recruiting� the underlying amygdala and or the hippocampus
Q: #158 How seisures Julia had, resulted from encephalatis with a bout of the mubms at age 2, influenced her behavior ?
A: Made her behavior very violent
Q: #159 What did EEG�s revelaed about termporal lobe and amygdala ?
A: Temporal lobe was malfunctioning; abnormalities in her left amygdala
Q: #160 Did lesioned in her left amygdala decreased her violent behavior ?
A: No
Q: #161 Did lesioned in her right amygdala decreased her violent behavior ?
A: Yes
Q: #162 What is the name of man who went up into the Observatory tower at the University of Texas and began shooting people walking across campus, killing 14 and then himself, Autopsy revealing a tumor the size off a walnut next to his amygdala, although, his diary indicated that he had planned this for a long time prior to the event and making this was not spontaneous aggression.
A: Charles Whitman
Q: #163 Were Amygdalectomies for the control of aggression in TLE patients successful ?
A: moderately succeseful
Q: #164 Were Amygdalectomies for the control of hyperactivity in children successful ?
A: less succeseful
Q: #165 @Clinical and physiological effects of stereotaxic bilateral amygdalotomy for intractable aggression.@ After surgery, both patients showed a [] in autonomic arousal levels to stressful stimuli and in the number of aggressive outbursts, although both patients continued to have difficulty controlling aggression. The "taming effect" reported after bilateral amygdalar destruction may be due to the amygdala's inadequate processing of perceived threat stimuli that would normally produce a fight-or-flight response. Stereotactic operation in behaviour disorders. Amygdalotomy and hypothalamotomy.
A: reduction
Q: #166 In 603 operations for control of conservatively untreatable aggressiveness: In 481 cases bilateral amygdalotomies and in 122 mostly secondary posteromedian hypothalamotomies have been performed. Initially excellent or moderate improvement was achieved in 76%. After a follow-up of more than three years this figure only slightly decreased to 70%. The group of patients who did not positively respond [] needs further study to discover the reasons for failure.
A: (30%)
Q: #167 @Aggression- Newer Modles@ What are the key 3 structures in the circuitry underlying emotion regulation in newer models ?
A: 1) on various sections of the prefrontal cortex -PFC -(orbital prefrontal -OFC; ventromedial and dorsolateral refrontal areas); 2) anterior cingulate cortex (ACC); 3) the amygdala.
Q: #168 Via what connection functions The mechanism underlying suppression of negative emotion ?
A: via an inhibitory connection from regions of the prefrontal cortex, probably the OFC, to the amygdala.
Q: #169 What irrespective of the distal cause, reflect abnormalities in the emotion regulation circuitry of the brain ?
A: Impulsive aggression and violence
Q: #170 What The OFC, through its connections with other zones of the PFC and with the amygdala, plays a crucial role in ?
A: constraining impulsive outbursts
Q: #171 What nerual system the ACC recruits in response to coflict ?
A: PFC