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Neuro > Synaptic Efficacy > Flashcards

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
Q

Hebbian

A

reflected in input specificity and associativity

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26
Q

GABAergic inhibition of postsynaptic cell

A

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

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27
Q

LTP induction requires: summary

A

Activation of NMDA receptors

Postsynaptic Ca 2+ release

Ca2 + acitvates kindase inclusing CaMKII which is necessary for LTP

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28
Q

two componnets of excitation

A

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
Q

NMDA r unlike AMPA r

A

can also let Ca2+ in
• Mg2+ block
• acts as a molecular coincidence detector ( as the key component )

30
Q

what can block LTP induction

A

can be used to chelate postsynaptic intra- cellular calcium levels

31
Q

unsilencing a synapse

A

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
Q

3 ways in which a synapse can be silent

A

Post: AMPAR silent

Pre: low Prob release, Gl release too low to produce quantal response ( Q )

33
Q

expression of LTP involves

A

unsilencing of synapse

conventional quantal analysis has failed to safely identify locus of expression

34
Q

EGTA blocks LTP induction revealing

A

calcium is necessary for induction

35
Q

synthetic peptide CaMKII

A

containing autoinhibitory domain of CAMKII

36
Q

CaMKII necessary for LTO induction

A

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
Q

activatoin of silent synapse by LTP induction could account for

A

both reduction in failures and changes in AMPARs

38
Q

candidate for retrograde signal

A

NO

need retrograde signal bcs is induction is post and maintenance is pre there must be a signal conveying this

39
Q

stimulating schaffer collateral at 1/s

A

leads to homosynaptic LTD

40
Q

homosynaptic LTD

A
  • NMDAr dependent
  • input specificity
  • can depotentiate already potentiated synapses
41
Q

potential mechanisms LTD

A

modest, prolonged rise in calcium concentration favors protein phosphatase - dephosphorylation - op- poses CaMKII activity - incline synapses towards LTD

42
Q

heterosynaptic LTD

A
  • LTP induction by tetan- isation of input fibres (closed circles) can induce LTD in adjacent synapses
43
Q

Using ACT-D to block protein synthesis

A

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
Q

Synaptic tagging hypothesis:

A
  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
Q

ocular dominance plasticity

A

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
Q

BCM Rule

A

BCM Rule (Bienenstock, Cooper, & Munro, 1982) = a sliding threshold (θm) for LTP or LTD induc- tion

frequency depenedent plasticity

47
Q

molecular basis of ocular dominance kitten

A

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
Q

hebbs neurophysiological postualte

A

spike timing-dependent plasticity ( STDP )

49
Q

why is timing of firing important

A

because of back-propagatoin of APs

Pre-before-post - LTP (. narrow range )

Post-before-pre - LTD ( broader more sensitive )

50
Q

spike-timing-dependent plasticity

A

Synaptic modification can encode temporal relation- ships

51
Q

slow wave sleep activity

A

up states –> stimulation LTD

down states –> LTD prevented because post follows pre

52
Q

synaptic stimulation up states

A

invariably led to NMDAR-dependent synaptic depression

unless postsynaptic neurone spiked within a nar- row time window following presynaptic stimula- tion

53
Q

advantages of up states synaptic stimulation

A
  1. improved S/N

2. preservation of previously stored input patterns

54
Q

activity dependent refinement of central synapses

A

frequency-dependent potentiation/depression

spike timing-dependent plasticity ( Hebbian )

sleep-associated plasticity

55
Q

learning

A

experience-dependent, relatively per- manent change in behaviour–> changed synaptic plasticity is one form of learning

56
Q

memory

A

persistence of learning

57
Q

gill reflex

A

Aplysia can be sensitised by stimu- lating tail using electric shocks

58
Q

sensitisation of stimulation

A

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
Q

long term and shorrt term facilitation relationship

A

long-term facilitation can be generated without short term facilitation

suggest use different 5-HT receptors

60
Q

classical conditioning

A

pairing a tail stimula- tion with or without a shock
• with shock - changed synaptic plasticity
• without shock - no change

61
Q

electric shock calcium channel mechanism

A

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
Q

inhibitory avoidance trianing

A

induces LTP

63
Q

discrimintative fear conditioning

A

induces LTP

  • increase in AMPAr current,
  • no difference NMDAR current
64
Q

no changed synaptic platicity

A

no changed behaviour

65
Q

hippocampus

A

necessary for spatial navigation rodents,

NMDAr blockers can impair spatial learning

66
Q

changed synaptic plasticity

A

necessary and sufficient to change behaviour

67
Q

auditory fear conditioning

A

requires LTP- if AMPAR insertion inhibited no fear conditioning

68
Q

how can fear memory be erased

A

by photostimulation of ACx/MGN neurones at 1Hz (low-frequency stimu- lation) to induce LTD

Neuro (13 decks)

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