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Synaptic Efficacy Flashcards

1
Q

synaptic efficacy

A

magnitude of postsynaptic resopnse ( change in membrane potential, second messenger activity ) to a given amount of presynaptic stimulation

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2
Q

synaptic plasticity

A

prolonged change in syn- aptic efficacy

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3
Q

how are EPP isolated for research

A

Curare can block AChRs to reduce amplitude of EPP below threshold for AP

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4
Q

quantal hypothesis

A
  1. spontaneous ‘miniature’ events
  2. Evoked response fluctuates in steps of unit size
    corresponding to size of ‘miniature’ events
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5
Q

observations of quantal release

A

using quantal analysis people have identified that a simple binomial release model fits obser- vations better than any Poisson distribution

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6
Q

paired-pulse facilitation

A

= postsynaptic re- sponse to second of a pair of presynaptic stimuli is greater than response to first

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7
Q

reasons for paired-pulse facilitation

A

presynaptic modification leading to increased release of neurotransmitter or ( under low ca2+ concentration )

increased postsynapitc response to given amounts of neurotransmitter

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8
Q

synaptic depression

A

efficacy can decrease

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9
Q

residual calcium hypothesis

A

when calcium does not fall to resting levels in presynaptic cell before second AP arrives

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10
Q

depression

A

vesicle depletion from the active zone

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11
Q

facilitation sensory

A

syt7 - CA1 pyramidal cell with which paired-pulse faciliation disappears

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12
Q

what is syt7 likely to faciliate

A

sytI dependent fusion of vesicles

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13
Q

temporal components

A

facilitation, augmentation, and post-tetanic potentiation (PTP)

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14
Q

LTP

A

a long-lasting en- hancement of synaptic efficiency induced by a brief period of high- frequency synaptic activation

can be generated by applying a tetanus to input fibres –> can last for weeks

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15
Q

single shock applied to input fibres

A

generate an evoked potential

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16
Q

examples of generating an evoked potential

A

perforant path for dentate gyrus,

schaffer collaterals for CA1 pyramidal cells

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17
Q

basic properties of LTP

A

cooperativity
input specificity
associativity

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18
Q

cooperativity

A
  • more nerve fibres stimulated (S2) - more likely to have LTP
  • intensity threshold for induction of LTP
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19
Q

input specificity

A

• stimulating S2 alone does not lead to S1 LTP
• other inputs not active at the time of tetanus do not share potentiation induced in tetanised
pathway

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20
Q

associativity

A

• stimulating S2 and S1 together lead to both S2 and S1 LTP

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21
Q

two major components of an EP

A

population EPSP

( initial slope can be used as an index of synaptic efficacy )

population spike

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22
Q

induction of LTP in dentate gyrus and CAI

A

mediated by NMDARs ( no LTP if blocked )

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23
Q

what happens to NMDARs during long term potentiation

A

normally blocked by MG2+ but simultanous binding of glutamate and depolarisation resleases MG 2+ block –> allows Ca2+ to flow in

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24
Q

what is needed for LTP induction

A

a rise in postsynaptic free Calcium ions ( no LTP without free Ca2+ )

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25
Hebbian
reflected in input specificity and associativity
26
GABAergic inhibition of postsynaptic cell
resists depolarisation caused by a single input pulse but weakens as a tetanus proceeds - stimulation must be strong and prolonged enough to induce LTP - reflected in cooperativity
27
LTP induction requires: summary
Activation of NMDA receptors Postsynaptic Ca 2+ release Ca2 + acitvates kindase inclusing CaMKII which is necessary for LTP
28
two componnets of excitation
AMPA and NMDA a. Depolarisation dislodges Mg2+ blocking NM- DARs - pure NMDA responses without AMPA b. (pairing = postsynaptic membrane was depolar- ises to -10mV) AMPAR component of EPSP is enhanced after LTP induction - suggests postsyn- aptic modification that selectively involves AM- PARs
29
NMDA r unlike AMPA r
can also let Ca2+ in • Mg2+ block • acts as a molecular coincidence detector ( as the key component )
30
what can block LTP induction
can be used to chelate postsynaptic intra- cellular calcium levels
31
unsilencing a synapse
Some synapses only NMDA during development --> silent synapses because no AMPA After initiating LTP --> unsilence synapse --> AMPA receptors inserted Key mechanism by which you get long term response this is one part of the story
32
3 ways in which a synapse can be silent
Post: AMPAR silent Pre: low Prob release, Gl release too low to produce quantal response ( Q )
33
expression of LTP involves
unsilencing of synapse conventional quantal analysis has failed to safely identify locus of expression
34
EGTA blocks LTP induction revealing
calcium is necessary for induction
35
synthetic peptide CaMKII
containing autoinhibitory domain of CAMKII
36
CaMKII necessary for LTO induction
if add protein synthesis blocker then a tetanus will induce a potentiation lasting about 30 mins but LTP does not occur • suggests that LTP involves a number of stages: 1. short-lasting potentiation (STP) 2. Later still requires proteins synthesis
37
activatoin of silent synapse by LTP induction could account for
both reduction in failures and changes in AMPARs
38
candidate for retrograde signal
NO need retrograde signal bcs is induction is post and maintenance is pre there must be a signal conveying this
39
stimulating schaffer collateral at 1/s
leads to homosynaptic LTD
40
homosynaptic LTD
- NMDAr dependent - input specificity - can depotentiate already potentiated synapses
41
potential mechanisms LTD
modest, prolonged rise in calcium concentration favors protein phosphatase - dephosphorylation - op- poses CaMKII activity - incline synapses towards LTD
42
heterosynaptic LTD
- LTP induction by tetan- isation of input fibres (closed circles) can induce LTD in adjacent synapses
43
Using ACT-D to block protein synthesis
suggests that protein synthesis is not required for early-phase LTP (induction) but for late-phase LTP (mainten- ance) required for full LTP - if blocked, potentiation returns to baseline within a few hours
44
Synaptic tagging hypothesis:
1. An LTP-inducing tetanus tags tetanised synapses, transiently potentiation them 2. It also induces protein synthesis - then diffuses cell wide to bind the tagged synapses - full LTP only in tagged synapses Illustration on the right: even if late-LTP in S2 is blocked by inhibition of protein synthesis, proteins synthesised due to late-LTP in S1 still tags synapse - potentiation
45
ocular dominance plasticity
occlusion of one eye during a sensitive period early in life causes some neurones in IVc to become activated only by the exposed eye * importantly, plasticity is blocked by injection of NMDAR blockers - * if occlusion reversed, pattern of ocular domin- ance gradually reverses too - metaplasticity
46
BCM Rule
BCM Rule (Bienenstock, Cooper, & Munro, 1982) = a sliding threshold (θm) for LTP or LTD induc- tion frequency depenedent plasticity
47
molecular basis of ocular dominance kitten
therefore, increase in NR2A/B ratio proposed to be responsible for sliding θm to the right to de- crease likelihood of synaptic strengthening visual experience absent - high constitutive ex- pression of NR2B (black subunits) and reduced expression of NR2A (white subunits) leads to an increase in NR1/NR2B diheteromeric receptors • visual experience present - increased NR2A ex- pression and rapid delivery of NR1/NR2A/ NR2B triheteromeric receptors to synapse, com- pensated by a net loss of surface NR1/NR2B di- heteromers
48
hebbs neurophysiological postualte
spike timing-dependent plasticity ( STDP )
49
why is timing of firing important
because of back-propagatoin of APs Pre-before-post - LTP (. narrow range ) Post-before-pre - LTD ( broader more sensitive )
50
spike-timing-dependent plasticity
Synaptic modification can encode temporal relation- ships
51
slow wave sleep activity
up states --> stimulation LTD down states --> LTD prevented because post follows pre
52
synaptic stimulation up states
invariably led to NMDAR-dependent synaptic depression unless postsynaptic neurone spiked within a nar- row time window following presynaptic stimula- tion
53
advantages of up states synaptic stimulation
1. improved S/N | 2. preservation of previously stored input patterns
54
activity dependent refinement of central synapses
frequency-dependent potentiation/depression spike timing-dependent plasticity ( Hebbian ) sleep-associated plasticity
55
learning
experience-dependent, relatively per- manent change in behaviour--> changed synaptic plasticity is one form of learning
56
memory
persistence of learning
57
gill reflex
Aplysia can be sensitised by stimu- lating tail using electric shocks
58
sensitisation of stimulation
presynaptic facilitation * 5-HT released from facilitating interneurone binds a GsPCR - activates AC to produce cAMP from ATP * cAMP activates PKA to phosphorylate S-type K channel (Calcium-gated) to allows voltage to remain relatively high for a longer time * Voltage-gated Ca2+ channels allow Ca2+ to come into presynapse to allow more vesicle re- lease
59
long term and shorrt term facilitation relationship
long-term facilitation can be generated without short term facilitation suggest use different 5-HT receptors
60
classical conditioning
pairing a tail stimula- tion with or without a shock • with shock - changed synaptic plasticity • without shock - no change
61
electric shock calcium channel mechanism
Electric shock opens Calcium channels, allow- ing Ca2+ to come in and bind to calmodulin, which becomes activated and binds to AC to produce cAMP
62
inhibitory avoidance trianing
induces LTP
63
discrimintative fear conditioning
induces LTP - increase in AMPAr current, - no difference NMDAR current
64
no changed synaptic platicity
no changed behaviour
65
hippocampus
necessary for spatial navigation rodents, | NMDAr blockers can impair spatial learning
66
changed synaptic plasticity
necessary and sufficient to change behaviour
67
auditory fear conditioning
requires LTP- if AMPAR insertion inhibited no fear conditioning
68
how can fear memory be erased
by photostimulation of ACx/MGN neurones at 1Hz (low-frequency stimu- lation) to induce LTD

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