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NEUR 310 > Synaptic Plasticity > Flashcards

Synaptic Plasticity Flashcards

1
Q

What is M=NPQ?

A

Formula for synaptic strength

P= Probability of release of a synaptic vesicle after an action potential (ranges from 0 to 1)
Q= Amplitude of the post-synaptic potential (PSP) resulting from the release of one vesicle.
N= number of vesicle release spots.
M is term for size of synaptic strength

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2
Q

What 3 factors can influence the probability of vesicle release?

A

Amount of Calcium entering with an action potential: More calcium, more release

Number of primed vesicles

Coupling of Calcium entry to fusion of the vesicle; More coupling, more release

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3
Q

What can be inferred from a readily releasable pool procedure (RRP)?

A

The RRP can be measured using an independent way of releasing vesicles, such as hypertonic shock that disrupts the membrane.
This releases all vesicles that are primed

PROVIDES A MEASURE OF P

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4
Q

How can P be modulated?

A

PPF, PPD, PTP, modulatory neurotransmission (e.g. STF in aplysia)

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5
Q

What determines whether paired pulse facilitation or depression occurs?

A

PPF occurs if initial probability of release is low
PPD occurs if initial probability of release is high

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6
Q

How can PPF be used to probe whether a change in synaptic strength results from a change in P or Q?

A

If there is increased synaptic strength but no change in PPF, it means that the underpinning change comes from Q, not P

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7
Q

If there is an increase in PPF, this means p _____
If there is a decrease in PPF, this means p _____
If there is no change in PPF, one can argue that p is _____.

A

If there is an increase in PPF, this means p decreased
If there is a decrease in PPF, this means p went up
If there is no change in PPF, one can argue that p is unchanged.

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8
Q

What is PPF due to?

A

residual calcium from previous firing

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9
Q

What sensor is mediating PPF? Why?

A

Syt 3 and 7 bc. sensitive to small amounts of calcium.

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10
Q

True or false: In PPF, calcium binding to just the Syt 7/Syt 3 releases VS.

A

False: Calcium binding to just the Syt 7/Syt 3 complexin site makes the vesicle more primed, but is not sufficient for fusion (need calcium binding to Syt 1,2,9 site as well)

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11
Q

What variable mainly influences PPD?

A

Time

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12
Q

True or false: The higher the probability of release, the more pronounced depression will be.

A

True, as more of the RRP will be secreted.

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13
Q

Is post-tetanic potentiation also relying on residual calcium?

A

Yes, indirectly

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14
Q

What are three calcium sensors involved in mediating PTP?

A

Munc13
PKC
Synaptotagmin 3

BUT THESE ARE CELL SPECIFIC

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15
Q

What does Syt3/7 increase during stimulus?

A

RRP

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16
Q

What is EGTA?

A

high affinity calcium sensory competing with Syt3 for clacium -> high affinity like Syt 7!!!

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17
Q

How can Munc13 increase RRP in PTP?

A

Munc13 binds calmodulin = calcium sensitivity -> calcium binding would accelerate Munc13’s ability to remove the inhibitory effect of Munc18 on syntaxin = increase in RRP

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18
Q

How can unc-13 be regulated to increase priming? Is it important for PTP?

A

DAG can bind to C1 domain of unc-13 and increase priming

PKC also phosphorylates both munc13 and munc18, promoting priming

YES

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19
Q

What is the time course of involvement of Munc13 and Syt3 during PTP?

A

During stimulus train Syt is important
Munc13 important afterward bc. binds calcium for longer

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20
Q

In terms of homeostasis, why are PPF and PTP important?

A

increasing probability of release when the neuron is firing is an attempt to keep p constant during a long train of action potentials

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21
Q

Short-term facilitation in aplysia is related to cellular habituation or sensitization?

A

Sensitization

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22
Q

Short-term facilitation is caused by an increase in P or Q?

A

P

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23
Q

Explain the cascade resulting in STF (from shock to release of transmitter)

A

Shock -> release of 5-HT -> G-prot -> cAMP -> PKA -> closing of K+ via phosphorylation -> slow repolarization after AP -> broader AP -> increase calcium influx -> more transmitter release

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24
Q

True or false: Amplitude of miniature EPSPS (minis) are most often probes for postsynaptic changes

A

Yes, but sometimes vesicle content can change (e.g., changing uptake rate)

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25
Q

RRP is increased after STF, what does that indicate?

A

In addition to be caused by a larger calcium influx, STF is also caused by increase in priming

26
Q

Is short term depression acting directly on RRP? How can it be reversed?

A

No, RRP is intact in depression -> therefore caused by a loss in calcium secretion coupling, which might be due to an untethering of the calcium channel and SV

PKC can restore calcium depression coupling at depressed synapses

27
Q

What properties are required of a physiological basis for memory

A

Persistence
Input Specificity
Associativity

28
Q

What kind of stimulation does it take to induce LTP?

A

Tetanic stimulation (100Hz) or Theta-Burst stimulation

29
Q

What molecular structure mediates the associativity of LTP?

A

NMDA receptors (coincidence detection)

30
Q

Why does LTP require calcium? And what allows the influx of calcium?

A

NMDA receptors allow Ca influx ->activation of CamKII

31
Q

How does LTP decrease failure rate?

A

By upregulating AMPA receptors in the postsynaptic neuron

32
Q

What is the evidence that LTP is not caused by increase in P?

A

Only increase in AMPA response (more vesicles released would not discriminate which receptor gets activated)

33
Q

How can LTP “unsilence” AMPA postsynaptic responses?

A

In synapses that express no AMPA receptors, expression of AMPA via NMDA increases the responsitivity of the postsynaptic neuron by 100% from 0%.

34
Q

What channel property of AMPA and NMDA allows to record NMDA currents almost entirely independently from AMPA currents?

A

AMAP currents shut off rapidly, while NMDA currents last longer -> simply wait for the AMPA currents to be off to record NMDA currents WITH magnesium block and CHANGING input voltage to separate NMDA (+40) and AMPA (-60) currents

35
Q

What is the pathway by which LTP leads to the insertion of more AMPA receptors

A

NMDA -> CamKII -> PKC -> substrate phosphorylation -> AMPA insertion

36
Q

How can you measure AMPA-R insertion during learning?

A

Use AUDITORY FEAR CONDITIONING = one-trial learning that takes place in the lateral amygdala where auditory inputs from the thalamus project

Need a way to distinguish newly inserted AMPA-Rs from previously present AMPA-Rs ->
ELECTROPHYSIOLOGICAL TAGGING – viral overexpression of GluA1 results in the formation of GluA1 homotetrameric AMPA- Rs that exhibit inward rectification. Normally AMPA-Rs are heterotetramers and non-rectifying.

37
Q

True or false: Preventing new GluA1 insertion was sufficient to prevent learning during fear conditioning.

A

True.

38
Q

How is L-LTP induced?

A

Multiple spaced trains of high-frequency stimulation

39
Q

What intracellular process does L-LTP require?

A

CREB activation and dendritic protein synthesis

40
Q

By which protein kinase is CREB phosphorylated by?

A

PKA

41
Q

L-LTP shows synapse specificity, how possible since in involves protein synthesis?

A

synaptic tagging:

L-LPT induces expression of “goodies” (plasticity related proteins)
+
Synapse would be tagged by initial AMPA trafficking event
= L-LTP

42
Q

What characterizes a successful synaptic capture in the case of L-LTP?

A

Strong L-LTP induction at synapse A = prod. of goodies + tag
Weak E-LTP induction at synapse B = no prod. of goodies + tag
Goodies expressed from strong L-LTP induction at synapse A will be capture BOTH by the tags of synapses A AND B

43
Q

What kind of stimulation provokes LTD?

A

Low freq. stimulation

44
Q

Is the downstream pathway of LTD similar to LTP?

A

Calcium is also needed in LTD, but afterward phosphatases and not kinases are the effectors

45
Q

How is LTD ultimately implemented?

A

Endocytosis of AMPA receptors

46
Q

What determines whether LTP or LTD occurs?

A

Intracellular concentration of calcium (det. by freq. of stimulation)
Kinases haev low. calcium affinity = requires a lot of calcium = intense stimulation = LTP
Phosphatases have high calcium affinity = requires a little bit a calcium = weak stimulation = LTD

47
Q

Which phosphatase is known to play a role in LTD?

A

Calcineurin

48
Q

Under which more realistic conditions than trains of stimulus are LTP and LTD happening? What is the name of the process?

A

Spike timing-dependent plasticity coordinates pre-synaptic activity with post-synaptic firing

49
Q

Pre- before post- results in ____
Post- before pre- results in ____

A

Pre- before post- results in LTP
Post- before pre- results in LTD

50
Q

What property of action potential is particularly important for spike timing-dependent plasticity?

A

Back propagation to the dendrites (synapse location)

51
Q

If 100% is the theoretical sum of calcium entry from EPSP and AP when measured independently, how much calcium do you get when:

AP comes before EPSP
EPSP comes before AP

A

AP (post) comes before EPSP (pre) = 50% = LTD
EPSP (pre) comes before AP (post) = 150% = LTP

52
Q

Are LTD postsyn or presyn at mossy fiber synapses? Provide respective pathway.

A

Presyn.
LTP = presyn. influx of Ca = activation of AC1 -> cAMP -> PKA = increase release prob.
LTD = glu retroactivating presyn. mGluR2 -> inhibition of AC1 -> cAMP -> PKA = decrease release prob.

53
Q

Is LTD at the cerebellar synapse (PC-PF) postsyn. or presyn.? Provide pathway. What is counter-intuitive about this mechanism?

A

Postsyn.
mGluR activation postsyn. -> PLC -> PKC -> phosphorylation (COUNTER-INTUITIVE) of AMPA receptors C-tails -> internalization of AMPAr

54
Q

Endocannabinoids usually increase or decrease transmitter release? Are they acting pre- or post-synaptically?

A

Endogenous cannabinoids are released presynaptically and act retrogradely on CB1 receptors to generate different forms of synaptic depression:

depolarization-dependent suppression of inhibition (DSI)
depolarization-dependent suppression of excitation (DSE)
LTD

55
Q

How is CB1 activation preventing presyn. transmitter release?

A

CB1 G prot. blocks calcium entry pre syn.

56
Q

Name one blocker of CB1r.

A

Rimonabant.

57
Q

What is the goal of homeostasis of neural activity?

A

Reach a target firing rate that lays between seizure and cell death

58
Q

With neuronal cultures, how can you demonstrate activity homeostasis?

A

Adding TTX, washing off = increase in spike activity
Adding bicuculline (GABA antagonist silencing inhibition, so increasing excitability), washing off = decrease in spike activity

59
Q

Is non-Hebbian plasticity (homeostasis) driven by change at specific synapses? On what molecular mechanism does it rely on? How does synaptic scaling relate to that?

A

No, whole circuit modification

Large scale trafficking of AMPA receptors

Synaptic scaling = all synapses of a regulated network conserve their relative synaptic strengths and are all regulated in the same manner (increase, decrease)

60
Q

Are NMDA receptors necessary for homeostatic plasticity?

A

No

61
Q

In inhibitory synapses, what receptors get regulated?

A

NEUR 310 (12 decks)

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