Term
| "Sending" neuron fires an _____ |
|
Definition
|
|
Term
|
Definition
| has a bunch of little presynaptic vesicles that contain neurotransmitters (the chemical messenger released at the synapse) |
|
|
Term
| dendrite of postsynaptic neuron is called the _____ |
|
Definition
|
|
Term
| junction between axon of presynaptic cell & dendrite of postsynaptic neuron = ? |
|
Definition
|
|
Term
| electrical signals that propagate down the axon go through a sort of transformation process where they are translated into a ______ signal |
|
Definition
|
|
Term
| how is chemical transmission more easily tuned compared to electrical? |
|
Definition
| how much or how little neurotransmitter is released |
|
|
Term
|
Definition
| a neuron can listen to a bunch of different inputs & based on all of those inputs, it can summate/integrate it all together before deciding which information to send |
|
|
Term
| how does chemical transmission give you some flexibility? |
|
Definition
| effect depends on which neurotransmitter is released (excitatory vs inhibitory) |
|
|
Term
| temporal control mechanism of chemical transmission |
|
Definition
| some release neurotransmitters very fast, some very slow |
|
|
Term
| the first chemical neurotransmitter that was really established was _____ |
|
Definition
|
|
Term
|
Definition
| German scientist who was trying to study/understand chemical transmission & its role in communication between neurons |
|
|
Term
| heart gets input from vagus nerve (axon of neuron found in the brainstem) & _____ is released here |
|
Definition
|
|
Term
|
Definition
| electrically stimulated vagus nerve --> slowing down of heart beating --> poured solution that the heart was sitting in into a vat that another heart was beating in --> when you pour the solution onto heart number two, it also slowed the heart down --> if you washed the solution out, the heart would speed back up |
|
|
Term
| where is acetylcholine particularly important? |
|
Definition
|
|
Term
|
Definition
| connects nervous system to muscular system |
|
|
Term
| even though not many neurons in the brain can make ACh, it is very important for _____ state |
|
Definition
|
|
Term
| what enzyme is necessary for the synthesis of ACh |
|
Definition
| cholineacetyltransferase (ChAT) |
|
|
Term
| reaction where you make ACh |
|
Definition
| acetyl coA + choline --> acetylcholine |
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|
Term
| if you have too much ACh, you have runaway muscle excitation --> ? |
|
Definition
| could lead to muscles locking up/paralysis |
|
|
Term
|
Definition
| ACh --> acetyl coA & coline |
|
|
Term
|
Definition
| one neuron, one neurotransmitter |
|
|
Term
| is there a limit on number of release sites/how many neurons a given neuron can contact? |
|
Definition
|
|
Term
| presynaptic terminal at the NMJ |
|
Definition
| motor neuron from brainstem |
|
|
Term
| postsynaptic side with receptors (determines the effect of the ACh) at the NMJ |
|
Definition
| the muscle (specifically the arm skeletal muscle) |
|
|
Term
|
Definition
|
|
Term
|
Definition
| indirectly gate ion channels that can influence the activity of the neuron |
|
|
Term
| junction between motor neurons & skeletal muscle |
|
Definition
|
|
Term
| why is the NMJ good to study? |
|
Definition
| in the periphery & easy to access |
|
|
Term
| NMJ releases a huge saturating amount of _____ |
|
Definition
|
|
Term
| stimulate axon of the NMJ --> ? |
|
Definition
| depolarization of muscle after about 2 - 3 ms that eventually tapers back down to baseline |
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|
Term
|
Definition
| depolarization that is a sub-threshold event (doesn't reach AP all-or-nothing threshold) |
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|
Term
|
Definition
|
|
Term
| EPSPs = change in the _____ of the postsynaptic neuron |
|
Definition
|
|
Term
| are nAChR's excitatory or inhibitory receptors? |
|
Definition
|
|
Term
| heart has _____ ACh receptors |
|
Definition
|
|
Term
| is ACh intrinsically excitatory? |
|
Definition
|
|
Term
| something that turns on a receptor |
|
Definition
|
|
Term
| something that turns off a receptor |
|
Definition
|
|
Term
| pre-synaptic cell of the NMJ |
|
Definition
|
|
Term
| post-synaptic cell of the NMJ |
|
Definition
|
|
Term
| neurotransmitter at the NMJ |
|
Definition
|
|
Term
| post-synaptic receptor at the NMJ |
|
Definition
|
|
Term
|
Definition
| when you expect to see a post-synaptic response when you stimulate a nerve |
|
|
Term
| really small events that just seem to spontaneously happen in terms of EPSPs --> ? |
|
Definition
| spontaneous EPSPs (sEPSPs) |
|
|
Term
| who discovered that neurotransmitters are released in vesicles (quantal packets of information)? |
|
Definition
| researchers studying sEPSP's (1952 by Fatt & Katz) |
|
|
Term
| put on an acetylcholinesterase inhibitor --> ? |
|
Definition
| response events got larger & decayed a lot slower |
|
|
Term
| what did Fatt & Katz notice about spontaneous responses? |
|
Definition
| they seem to have discrete sizes |
|
|
Term
| smallest event Fatt & Katz ever saw |
|
Definition
|
|
Term
|
Definition
1. ACh
2. nicotine
3. carbachol |
|
|
Term
|
Definition
1. neostigmine
2. sarin nerve gas |
|
|
Term
|
Definition
1. curare - competitive antagonist
2. alpha-bungarotoxin - non-competitive antagonist |
|
|
Term
| pre-synaptic terminal contains vesicles which contain the _____ |
|
Definition
|
|
Term
| vesicles can dock with the inside of the pre-synaptic surface facing the ______ |
|
Definition
|
|
Term
| sometimes vesicles release too early --> ? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| are evoked EPSPs larger or smaller than an mEPSP? |
|
Definition
|
|
Term
| the probability of release (p) can be changed by changing ______ |
|
Definition
| extracellular calcium levels |
|
|
Term
|
Definition
|
|
Term
| can an axon of a presynaptic cell attach to postsynaptic cell at multiple branching sites? |
|
Definition
|
|
Term
| discrete size of EPSPs --> Fatt & Katz observed a _____ distribution describing release of synaptic vesicles |
|
Definition
|
|
Term
| Fatt & Katz put neurons in an environment where they are very unlikely to release vesicles (low calcium) so they could _____ |
|
Definition
| really study just 1 or 2 at a time |
|
|
Term
| a ton of receptors --> a big or small mini? |
|
Definition
|
|
Term
| small amount of receptors --> a big or small mini? |
|
Definition
|
|
Term
| size of a mini is also referred to as the _____ |
|
Definition
|
|
Term
| how can a mini EPSP be an evoked EPSP? |
|
Definition
| you put the cell in an environment where they are likely to only release one vesicle & then stimulate it presynaptically |
|
|
Term
| will "n" (amount of vesicles available at the synapse) always be a whole number? |
|
Definition
|
|
Term
| is "n" (amount of vesicles available at the synapse) fixed? |
|
Definition
|
|
Term
| does "m" (on average, how many vesicles are released when there is an AP) need to be a whole number? |
|
Definition
|
|
Term
| equation relating "m", "p", & "n" |
|
Definition
|
|
Term
|
Definition
|
|
Term
| quantal size (q) is specifically helpful telling you about ______ |
|
Definition
| post-synaptic sensitivity |
|
|
Term
| different quantal size is related to different ______ |
|
Definition
| amounts of receptors on the post-synaptic cell |
|
|
Term
| looking at a graph of EPSP amp vs number of observations --> quantal size will be ______ |
|
Definition
| first peak that you see not at 0 (EPSP amp of this peak) |
|
|
Term
| the only thing that changes quantal size is ______ |
|
Definition
| post-synaptic sensitivity |
|
|
Term
|
Definition
|
|
Term
| equation for EPSP amplitude, q, and m |
|
Definition
| EPSP amplitude (mV) = q * m |
|
|
Term
| skews of quantal analysis graphs: weak |
|
Definition
|
|
Term
| skews of quantal analysis graphs: average |
|
Definition
| fairly normal distribution |
|
|
Term
| skews of quantal analysis graphs: strong |
|
Definition
|
|
Term
| neurotransmitter release via ______ fusion with the presynaptic terminal |
|
Definition
|
|
Term
| neurotransmitter gets synthesized in the _______ |
|
Definition
|
|
Term
| neurotransmitter gets packaged into little ______ |
|
Definition
|
|
Term
| vesicle transport molecules |
|
Definition
| move them around where they need to go |
|
|
Term
|
Definition
1. reserve pool: vesicles just kind of hanging out in the presyantpic terminal but not in the exact position to be ready to be sent out in response to calcium influx
2. readily-releasable pool: vesicles able to be released right when calcium comes in |
|
|
Term
|
Definition
| docked vesicles to the membrane |
|
|
Term
|
Definition
| moving vesicle from reserve pool to be primed for release & moved to the membrane |
|
|
Term
| calcium comes in through ______ for vesicle release |
|
Definition
| voltage-gated calcium channels |
|
|
Term
| ______ interacts with docked vesicles & causes them to be released |
|
Definition
|
|
Term
| formation of ______ complex is required to dock vesicles |
|
Definition
|
|
Term
| when a vesicle is ______, it is anchored to the presynaptic membrane |
|
Definition
|
|
Term
| 2 types of SNAREs that interact to hold vesicle in place |
|
Definition
|
|
Term
| until it is ready to fuse, ______ actively blocks the vesicle fusion that would lead to neurotransmitter release |
|
Definition
|
|
Term
| entering calcium binds to synaptotagmin --> ? |
|
Definition
| calcium bound syanptotagmin catalyzes membrane fusion |
|
|
Term
|
Definition
|
|
Term
| the different kinds of synaptotagmin have different sensitivities to calcium --> ? |
|
Definition
| influences probability of release |
|
|
Term
| basically, if there is more ______ you are more likely that it will bind to synaptotagmin to allow for vesicle release |
|
Definition
|
|
Term
| if presynaptic membrane is depolarized beyond activation voltage for voltage-gated calcium channels (about -50 mV), what happens? |
|
Definition
| calcium comes in & diffuses around presynaptic area |
|
|
Term
| 4 steps following if calcium binds to synaptotagmin |
|
Definition
1. vesicle fusion
2. neurotransmitter release
3. binds with postsynaptic receptors
4. postsynaptic depolarization |
|
|
Term
| what destroys SNARE proteins |
|
Definition
|
|
Term
| full name for black widow spider venom |
|
Definition
|
|
Term
| what makes pores in the membrane for calcium entry |
|
Definition
|
|
Term
| presynaptic depression paired pulse ratios --> ? |
|
Definition
| smaller response in second pulse |
|
|
Term
| presynaptic facilitation paired pulse ratios --> ? |
|
Definition
| higher response in second pulse |
|
|
Term
| what does it mean that paired pulse ratios reveal presynaptic dynamics? |
|
Definition
| tells you whether it is a high or low probability of release synapse |
|
|
Term
| 2 ways to change the strength of a synapse |
|
Definition
1. change presynaptic vesicle release probability (more neurotransmitter --> strengthen synapse)
2. change number of postsynaptic receptors (more receptors --> strengthen synapse) |
|
|
Term
| give two electrical pulses to the nerve in rapid succession (50 ms) & the second EPSP is smaller = ? |
|
Definition
|
|
Term
| is short-term depression the same thing as LTD? |
|
Definition
|
|
Term
| why is the second EPSP smaller than the first EPSP in short-term depression? |
|
Definition
| depletion of readily releasable pool |
|
|
Term
| equation for paired pulse ratio (PPR) |
|
Definition
|
|
Term
| if you have a high probability of release (ex. 0.8) --> in paired pulse? |
|
Definition
| more vesicles will be released at the first pulse & there are very few docked vesicles left in the readily releasable pool for release |
|
|
Term
| when you see _______, it implies that the initial probability of release at that synapse is high |
|
Definition
|
|
Term
| what is indicative of synapses with an initially low probability of release |
|
Definition
|
|
Term
| you give a pulse & then you give another pulse 50 ms later (very soon!) --> ? (short term facilitation) |
|
Definition
|
|
Term
| if you have a lot of ______ around, you will probably get neurotransmitter release because it is more likely to bind to synaptotagmin to move it out of the way |
|
Definition
|
|
Term
| if you don't have a lot of calcium around, there will be a not very strong coupling of calcium influx to ______ |
|
Definition
|
|
Term
| short-term facilitation second pulse gives extra boost to calcium already there --> ? |
|
Definition
| more likely to bind to synaptotagmin to release vesicles |
|
|
Term
| the boosted calcium amount has more vesicles to interact with if there is a ______ probability of release on the first pulse |
|
Definition
|
|
Term
| short-term faciliation --> ______ in second pulse |
|
Definition
|
|
Term
| short-term depression --> ______ in second pulse |
|
Definition
|
|
Term
| short-term depression --> initial ______ prob of release |
|
Definition
|
|
Term
| short-term facilitation --> initial ______ prob of release |
|
Definition
|
|
Term
| synapse with mixed facilitation & depression could happen because? |
|
Definition
1. second pulse increases effective concentration of calcium & enough vesicles are still docked that second pulse causes release of more vesicles than first pulse
2. continued stimulation of synapse causes readily releasable pool of vesicles to become progressively more depleted, so even though calcium concentration is still high, fewer vesicles are released |
|
|
Term
| myasthenia gravis symptoms |
|
Definition
| weakness of muscles that are frequently used |
|
|
Term
| autoimmune disease where body makes antibodies against post-synaptic nicotinic ACh receptors at NMJ |
|
Definition
|
|
Term
| does myasthenia gravis affect presynaptic terminals? |
|
Definition
| no! but you have a finite number of post-synaptic receptors |
|
|
Term
| myasthenia gravis on a synaptic physiology level: decrease in size of mini EPSP --> ? |
|
Definition
| decrease in size of average EPSP |
|
|
Term
| muscles become weak with repetitive use in myasthenia gravis because ______ |
|
Definition
| depression is starting from a lower starting point |
|
|
Term
| treatment of myasthenia gravis |
|
Definition
|
|
Term
| autoimmune disease where body makes antibodies against presynaptic calcium channels of the NMJ |
|
Definition
|
|
Term
|
Definition
|
|
Term
| what you see at a LEMS synaptic physiology level |
|
Definition
| you would see many more "failures" on quantal analysis graph |
|
|
Term
| you actually get better with muscle use in LEMS because more use --> ? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| myasthenia gravis vs LEMS: cause |
|
Definition
| both autoimmune disorders |
|
|
Term
| myasthenia gravis vs LEMS: symptoms |
|
Definition
myasthenia gravis: muscle weakness particularly in muscles with repetitive use (ex. drooping eyelids, chewing muscles, etc.)
LEMS: muscle weakness but the weakness is moreso after you've been sitting for a long time |
|
|
Term
| why are the symptoms of myasthenia gravis & LEMS different? |
|
Definition
if you record from muscle in MG patient, there is an initial strong response but with repeated use, the postsynaptic nAChRs get bound up & receptor loses its efficacy
LEMS postsynaptic response starts really small & gets bigger because calcium builds up in presynaptic terminal with more & more APs --> eventually you get enough for a normal ACh release |
|
|
Term
| both myasthenia gravis & LEMS result from poor communication/connection between pre- and postsynaptic terminals in NMJ...______ is just a postsynaptic issue & ______ is a presynaptic issue |
|
Definition
|
|
Term
| treatment for both myasthenia gravis & LEMS is ______ |
|
Definition
| acetylcholinesterase inhibitors (such as neostigmine) |
|
|
Term
| one of the most ubiquitous synapses in the CNS = ? |
|
Definition
|
|
Term
| is glutamate inherently excitatory? |
|
Definition
|
|
Term
| if a neuron synthesizes _____, it will have a VGLUT |
|
Definition
|
|
Term
| if a neuron is postsynaptic for _______, it will have AMPA and/or NMDA glutamate receptors |
|
Definition
|
|
Term
| _______ synapses will have astrocytes (glial cells) |
|
Definition
|
|
Term
|
Definition
| excitatory post-synaptic potentials |
|
|
Term
|
Definition
| excitatory post-synaptic currents |
|
|
Term
| _______ glutamatergic receptors are controlled by the presence of glutamate, not voltage |
|
Definition
|
|
Term
| AMPA & NMDA are both ______ glutamate receptors |
|
Definition
|
|
Term
| AMPA vs NMDA: ions they allow to flow |
|
Definition
AMPA = sodium into the cell
NMDA = sodium into the cell & also calcium into the cell |
|
|
Term
|
Definition
AMPA: glutamate, AMPA (synthetic molecules)
NMDA: glutamate, NMDA (synthetic molecules) |
|
|
Term
| do almost all glutamate receptors have just AMPA, just NMDA, or both? |
|
Definition
|
|
Term
| AMPA vs NMDA: antagonists |
|
Definition
AMPA: QX compounds (DNQX, CNQX, NBQX)
NMDA: APV (AP5), MK801 (will only bind & inactivate NMDA receptors once they have been opened at least once) |
|
|
Term
|
Definition
AMPA: linear (think: like a leak channel...flow of ions completely follows Ohm's Law --> current will always be directly related to driving force)
NMDA: non-linear (because they have an intracellular magnesium block) |
|
|
Term
| AMPA vs NMDA: ion permeability |
|
Definition
AMPA: sodium & potassium (mostly sodium)
NMDA: sodium & potassium (mostly sodium) & also calcium |
|
|
Term
|
Definition
AMPA: very fast
NMDA: very slow |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| NMDA has ______ kinetics than AMPA |
|
Definition
|
|
Term
| Why is there all the weird stuff going on for NMDA IV plot when the cell is more hyperpolarized than 0? |
|
Definition
| magnesium is a positively charged ion --> at hyperpolarized voltages, the magnesium will be bound into the pore of the NMDA receptor --> no current can go through |
|
|
Term
| What would NMDA IV plot look like without magnesium block? |
|
Definition
|
|
Term
| at -80 mV, you will see a current in response to glutamate, but it is purely an _______ current |
|
Definition
|
|
Term
| NMDA receptors don't start to get involved until around _____ mV |
|
Definition
|
|
Term
| If you see a difference in current in the presence of APV, you are blocking the ______ current because it can only come in through the NMDA receptors (also you will get less sodium but mainly demonstrating the loss of this current) |
|
Definition
|
|
Term
| ______ require both glutamate & postsynaptic depolarization to allow current to come through the cell |
|
Definition
|
|
Term
|
Definition
| presynaptic activity & postsynaptic activity |
|
|
Term
| coincidence detection in NMDA receptors is caused by _______ |
|
Definition
|
|
Term
| ______ is required for LTP! |
|
Definition
|
|
Term
| ______ receptors are only active when neuron is active (i.e. depolarized) |
|
Definition
|
|
Term
| the molecular mechanism that allows learning to happen |
|
Definition
| NMDA receptors are coincidence detectors that allow calcium influx only when neurons are depolarized |
|
|
Term
| very short time scale (10 ms - 1 s) + strengthened = ? |
|
Definition
|
|
Term
| very short time scale (10 ms - 1 s ) + weakened = ? |
|
Definition
| synaptic depression (short-term depression) |
|
|
Term
| medium length time scale (hours) + strengthened = ? |
|
Definition
| long-term potentiation (LTP) |
|
|
Term
| long length time scale (days) + strengthened = ? |
|
Definition
|
|
Term
| long length time scale (days) + weakened = ? |
|
Definition
|
|
Term
| the ability of synapses to strengthen or weaken over time in response to increases or decreases in their activity |
|
Definition
|
|
Term
| "Plasticity" just means _______ |
|
Definition
|
|
Term
| the canonical mechanism of cellular learning in the brain |
|
Definition
|
|
Term
| describe the specificity of LTP |
|
Definition
| if you have a neuron that is getting input from two different presynaptic cells, the one that is releasing glutamate coincident in time to postsynaptic activity --> strengthening in that synapse compared to the other presynaptic cell |
|
|
Term
| describe associativity of LTP |
|
Definition
| once you have a strong connection in one synapse, others that fire when that one fires (even if they are weaker) onto the same postsynaptic neuron will have an association strengthening with that initial strong presynaptic neuron |
|
|
Term
| the hippocampus has been known for a long time to be important for ______ |
|
Definition
|
|
Term
|
Definition
| to fix his epilepsy, a surgeon lesioned his hippocampus --> HM was no longer able to form new memories |
|
|
Term
| If you can't do LTP in the hippocampus, you cannot ______ |
|
Definition
|
|
Term
| experiment discovering LTP |
|
Definition
| tetanic stimulation --> huge vesicle release (huge depolarization of hippocampal pyramidal neuron) --> waited a bit & then gave a single pulse --> much larger postsynaptic response compared to responses before tetanic stimulation |
|
|
Term
|
Definition
1. huge amount of depolarization
2. magnesium block comes out of NMDAR
3, calcium flows into the cell
4. calcium activates CaMKII (calcium-calmodulin-dependent protein kinase II)
5. CaMKII phosphorylates target proteins |
|
|
Term
| NMDARs provide the ______, but they do not change in number or really contribute to the size of the response |
|
Definition
|
|
Term
| ______ is essentially the "memory molecule" |
|
Definition
|
|
Term
| how do groups of CaMKII molecules act? |
|
Definition
| hang out together & can cooperate with each other in a holoenzyme complex |
|
|
Term
| calcium binds to calmodulin --> ? |
|
Definition
| calmodulin binds to CaMKII to activate it by changing its conformation |
|
|
Term
| eventually, calcium & calmodulin will disassociate BUT CaMKII can continue to phosphorylate itself at site ______ |
|
Definition
|
|
Term
| Can mice with mutations in CaMKII learn the Morris Water Maze? |
|
Definition
|
|
Term
| what happens in control mice in the Morris Water Maze? |
|
Definition
| eventually, they learn exactly where platform is & will find platform very quickly (4 - 5 training sessions!) |
|
|
Term
| a strengthening of the synaptic connection between two neurons |
|
Definition
|
|
Term
| when you look at a graph showing LTP, you are basically looking at ______ currents |
|
Definition
|
|
Term
| APV (AP5) has what effect on LTP? |
|
Definition
|
|
Term
|
Definition
| compound that blocks CaMKII activity |
|
|
Term
| normal autophosphorylation keeps CaMKII active for up to an hour after calcium influx --> ? |
|
Definition
| driving of AMPARs into postsynaptic terminal |
|
|
Term
| what does a current graph look like when you prevent CaMKII autoP to block LTP? |
|
Definition
| like using APV, you still get the 100% next to baseline AMPAR current but you just don't get the LTP increase that you see normally following tetanic stimulation |
|
|
Term
| aplysia gill withdrawal reflex |
|
Definition
| normal aplysia will pull in siphon/gills if touched but will come back out after about 10 seconds |
|
|
Term
| 5 steps in aplysia gill withdrawal reflex |
|
Definition
1. sensory neurons have dendrites in siphon
2. sensory neuron releases glutamate onto motor neuron in response to siphon being poked
3. motor neuron causes muscles in gill to retract to protect the gill
4. maintain sucked in position for about 10 seconds
5. relax back |
|
|
Term
| touch the siphon --> ______ in motor neuron |
|
Definition
|
|
Term
| what happens if you teach the aplysia that touching the siphon comes along with a shock? |
|
Definition
| every time you touch the siphon --> electric shock on tail --> induce plasticity between sensory & motor neuron (presynaptic strengthening) --> touching the siphon even without shock, you get a much stronger gill withdrawal reflex than before |
|
|
Term
| sensory neuron from aplysia tail activates ______ in response to shock |
|
Definition
|
|
Term
| facilitating interneuron has 5HT --> ? |
|
Definition
| when it is activated 5HT is released onto axon terminal of siphon sensory neuron |
|
|
Term
| 6 molecular mechanisms of short-term facilitation |
|
Definition
1. 5HT release onto siphon sensory neuron
2. metabotropic receptor binds 5HT
3. couples to intracellular signaling pathways (GPCR)
4. G protein dissociates from receptor to target adenylyl cyclase
5. makes cyclic AMP (cAMP) second messenger to trigger many intracellular changes
6. activates protein kinase A (PKA) (AKA "cyclic AMP-dependent protein kinase) |
|
|
Term
| 3 possible outcomes of activating PKA |
|
Definition
1. increases readily releasable pool of neurotransmitters/vesicles
2. phosphorylate voltage-gated calcium channels
3. phosphorylate voltage-gated potassium channels |
|
|
Term
| Is PKA relevant for human learning & memory? |
|
Definition
|
|
Term
| does PKA increase or decrease potassium current? |
|
Definition
|
|
Term
| 3 steps for changing potassium current to increase neurotransmitter release |
|
Definition
1. decrease potassium current
2. changes shape of the AP
3. spends more time depolarized in response to AP which allows calcium in which leads to vesicle release |
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|
Term
| PKA gets activated by cAMP which gets produced when ______ |
|
Definition
| 5HT binds to GPCRs on siphon sensory neuron |
|
|
Term
| more glutamate release from siphon sensory neuron onto motor neuron --> ? |
|
Definition
| increased gill withdrawal reflex |
|
|
Term
| do the same molecular cascades go on to produce a long-term vs a short-term memory? |
|
Definition
|
|
Term
| how does structural plasticity work for long-term potentiation? |
|
Definition
| you are actually causing growth of new connections between sensory neuron & motor neuron! |
|
|
Term
|
Definition
| regulatory subunits (2) and catalytic subunits (2) |
|
|
Term
| what happens to the regulatory subunits & catalytic sites when cAMP activates PKA? |
|
Definition
| regulatory subunits dissociate from the catalytic sites |
|
|
Term
| what happens when PKA is active for a long time? |
|
Definition
| it actually trans-locates up the axon to the nucleus of the cell |
|
|
Term
| when in the nucleus, PKA activates ______ |
|
Definition
|
|
Term
| 4 steps how phosphorylation of CREB turns on gene transcription |
|
Definition
1. cAMP turns on PKA
2. repeated long-term activation PKA translocates to nucleus
3. PKA phosphorylates CREB
4. long-term memories are formed due to change in gene transcription |
|
|
Term
|
Definition
| memory storage for emotional events |
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|
Term
| mutations in ______ block long-term fear conditioning |
|
Definition
|
|
Term
| is short term memory fine in a CREB mutant? |
|
Definition
|
|
Term
|
Definition
| protein synthesis inhibitor |
|
|
Term
|
Definition
|
|
Term
| PKA travels to the nucleus, leads to _______ |
|
Definition
|
|
Term
| phosphorylation of CREB leads to ______ |
|
Definition
|
|
Term
| 2 results that are the same whether you block CREB phosphorylation or protein synthesis |
|
Definition
1. short term memory is fine
2. long term memory is hindered |
|
|
Term
| blocking NMDA receptors prevents any ______ |
|
Definition
|
|
Term
| preventing CaMKII autoP blocks ______ |
|
Definition
|
|
Term
| CREB mutant: short-term vs long-term change |
|
Definition
| facilitation in beginning but no long term change because no gene expression changes in the nucleus (transcription factor is not active) |
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|
Term
| block CREB or protein synthesis --> ? |
|
Definition
| protein/plasticity that fades within a few hours |
|
|
Term
|
Definition
| EPSP slope never really leaves baseline |
|
|
Term
| ACT-D or anisomycin --> ? |
|
Definition
| field EPSP slope jumps up initially, but then fades back to baseline |
|
|
Term
| increase in connection between two neurons (more synapses) |
|
Definition
|
|
Term
| more axon branches are made & synapse onto dendrite of neuron with ______ |
|
Definition
|
|
Term
|
Definition
| brain derived neurotrophic factor (axon growth) |
|
|
Term
|
Definition
| activity-related cytoskeletal associated protein |
|
|
Term
|
Definition
| transcription factor that regulates other genes |
|
|
Term
| ______ can be used to label neurons during a memory task |
|
Definition
|
|
Term
| hypothesis of what is a memory |
|
Definition
| a memory is just a specific grouping of neurons that are activated at the same time (called an engram) |
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|
Term
| if we activate a "memory" we should be able to see evidence of _______ in a group of neurons (cfos) |
|
Definition
|
|
Term
| if cfos labeled neurons are really a memory, & we can somehow use optogenetics, we should be able to ______ |
|
Definition
| turn that memory on & off |
|
|
Term
|
Definition
| cluster of neurons active at the same time, constitutes a memory |
|
|
Term
| for optogenetics, we use a viral injection to insert new _____ into the cell membrane |
|
Definition
|
|
Term
| new proteins inserted in optogenetics |
|
Definition
| light-activated ion channels (opsins) |
|
|
Term
| channelrhodopsin (ChR2) ______ neurons |
|
Definition
|
|
Term
| archaerhodopsin (Arch) ______ neurons |
|
Definition
|
|
Term
| Arch-T activation of tagged neurons --> ? |
|
Definition
| NOT freezing when placed in the context |
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|
Term
| ChR2 activation of tagged neurons --> ? |
|
Definition
| freezing in a new context |
|
|
Term
|
Definition
|
|
Term
| paired pulse test --> 2 possible evoked responses |
|
Definition
1. facilitation
2. depression |
|
|
Term
| presynaptic causes of facilitation vs depression |
|
Definition
facilitation: not many vesicles were released with the first pulse; more calcium needed to enter the terminal (serotonin --> PKA --> increase calcium influx)
depression: the pool of readily-releasable vesicles was depleted with the first pulse |
|
|
Term
| short-term memory is commonly considered ______ |
|
Definition
|
|
Term
| postsynaptic causes of LTP |
|
Definition
| NMDA receptors as a coincidence detector; leads to activation of CaMKII |
|
|
Term
| long-term memory is considered ______ |
|
Definition
|
|
Term
| presynaptic causes of L-LTP |
|
Definition
| serotonin receptors lead to phosphorylation of CREB through GPCR signaling cascade; requires the nucleus (in the soma) |
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