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PHOL009 > LTP/LTD/STDP > Flashcards

LTP/LTD/STDP Flashcards

1
Q

Hebb’s postulate? (and when)

A

When an axon of cell A is near enough to excite a cell B and repeatedly or persistently take part in firing it, some growth process/metablic change takes place in one/both cells such that A’s efficiency, as one of the cells firing B, is increased

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2
Q

How can this requirement for correlated pre- and postsynaptic synaptic activity be interpreted?

A

Requirement for convergent and synchronous activity (presynaptic)

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3
Q

What did Terje Lomo observe (and when)? (+ref)

A

Persistent increase in synaptic strength after pairing pre- and postsynaptic activity (1966) - Bliss & Lomo, 1973

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4
Q

What did early studies of EC-GC synapses show identify? (+ref)

A

Features of a Hebb synapse - ability for long-term increases/decreases in synaptic strength (Levy and Stewart. 1979)

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5
Q

What else does the Hebb synapse require?

A

Coactivity of a number of presynaptic elements to induce such changes

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6
Q

Cooperativity?

A

A weak input, in which only a few excitatory synapses were tetanize, failed to induce LTP, whereas a strong input reliably induced LTP

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7
Q

What was only seen in the tetanized pathway? (and what does this demonstrate)

A

A strong input reliably induced LTP, but only in the tetanized pathway (“input specificity”)

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8
Q

Associativity?

A

Simultaneous activation of two seperate inputs, one of which is weak and fails to undergo LTP on its own, exhibits robust LTP when tetanized together with a strong input

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9
Q

What did Levy and Steward (1983) find?

A

Changes in synaptic efficacy (EC-DG) dependent on the temporal order of the input stimuli

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10
Q

What did potentiation/depression result from? What was this the first evidence for?

A

When the LFS preceded HFS by less than 20 ms (and reverse led to weakening) - first evidence for sensitivity of synaptic modification to relative timing of pre- and postsynaptic spikes

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11
Q

What did Markram verify (and when)?

A

The significance of the relative timing + defined a critical window for the coincidence detection (10s of milliseconds) - 1997

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12
Q

What does the temporal requirement for STDP depend on?

A

Preparation, brain area, cell types and dendritic location - classical form = excitatory glutamatergic synapses in HPC

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13
Q

What produces maximal synaptic modification?

A

Small differences between pre- and postsynaptic spikes produce maximal synaptic modification (no plasticity observed when difference is too large)

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14
Q

Relative order determines LTP/LTD: ref?

A

Abbot and Nelson, 2000

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15
Q

What is the requirement of causality further reinforced by?

A

The exponential decay in the amount of LTP, which restricts the potentiation to the spikes arriving within the temporal window during which a neuron is able to integrate inputs

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16
Q

What does the fact that STDP restricts plasticity to active synapses exemplify?

A

Input-specificity of Hebbian plasticity

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17
Q

How does STPD expand Hebb’s original hypothesis?

A

Cells that fire together can wire together or unwire, depending on the timing between cells A and B

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18
Q

What does STDP also address?

A

More temporally sensitive computation tasks, while adding stability to neural networks

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19
Q

What does the Hebbian model assume, and what does this lead to?

A

That LTP/LTD occur independently at each synapse, which can lead to instability in the form of excessively low or high firing rates,

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20
Q

How does STDP provide a source of stability for recurrent networks without leading to runaway excitation? (+ ref)

A

By enforcing a specific temporal order, synapses from the presynaptic to postysnaptic neuron are strengthened while those in the opposite order will be weakened (Gilson et al., 2010)

21
Q

The NMDAR is believed to act as a coincidence detector… (+ref)

A

….allowing the influx of Ca2+ following the presynaptic release of glutamate and coincident postsynaptic depolarisation that results in the removal of the MG2+ block (Mayer et al., 1984)

22
Q

What does the cooperativity threshold of LTP arise from? (+ explanation for why weak stimulus doesn’t produce LTP)

A

From the need for depolarisation to reduce the level of block (weak stimuli activating only a few afferent fibres fail to induce LTP because the resulting level of depolarisation does not produce adequate reduction in the block)

23
Q

When does depolarisation spread between neighbouring synapses?

A

Many fibres activated in synchrony by a strong stimulus (enhances unblocking of NMDARs)

24
Q

Calcium hypothesis? (+ref)

A

Depending on stimulation, two distinct types of Ca2+ signals can arise - separate downstream pathways (Artola and Singer, 1993)

25
Q

What does the intracellular rise in Ca2+ after HFS promote?

A

Activation of CaMKII followed by LTP induction

26
Q

What does LFS result in? (+ref)

A

More gradual rise in Ca2+ that leads to the recruitment of phosphatase, e.g. PP1 and calcineurin (Yang et al., 1999)

27
Q

Proposed mechanism for LTP? (+ref) [residue!]

A

Phosphorylation of Ser831 of GluA1 by CaMKII, enahancement of their transmission + strengthening of synapse (Malinow and Malenka, 2002)

28
Q

What else is involved in synaptic modification? (+ref)

A

Postsynaptic TrkB receptors which can increase NMDAR conductance to upregulate Ca2+ influx (Figurov et al., 1996)

29
Q

What else is proposed to be triggered by the influx of calcium ions? (+ref)

A

Downstream signalling pathways, such as the positive feedback loop following mTOR-dependent translation of the neurotrophin BDNF which stimulates presynaptic transmitter release, while postsynaptically interacting with TrkBRs to increase phosphorylation of NMDARs (Hao et al., 2018)

30
Q

What does this lead to (BDNF, TrkB..)? (+ref)

A

Increase in the open probability while facilitating synaptic clustering and AMPAR upregulation (Caldeira et al., 2007)

31
Q

What have APs been shown to do once initiated? (+ref)

A

Spread through the dendritic tree in a retrograde manner (Stuart et al. 1997)

32
Q

What does a bAP represent and what is it believed to serve?

A

Represents the integrated sum of all (active) presynaptic inputs onto a neuron and is believed to serve as a specialised associative signal that can facilitate the removal of the Mg2+ block + activity-depednent influx of Ca2+

33
Q

What does the bAP promote? (+ref)

A

Modification of dendritic synapses that contributed to the inititiation of the AP (Markram et al., 1997)

34
Q

What other mechanism could explain the narrow window for coincidence detection?

A

Kinetics of Mg2+ unblock

35
Q

What does the voltage-dependence associated with the Mg2+ unblock mean?

A

Synaptic currents are prolonged when the membrane is depolarised, which can facilitate LTP through the enhancement of NMDAR conductance

36
Q

What does the time-dependence of the unblock lead to? (+ref)

A

Sharpening of the window for coincidence detection and induction of STDP (Kampa et al., 2004)

37
Q

Where does another influence on the window for LTP induction arise from?

A

Interactions between the bAP and EPSP, which can promote changes in active dendritic conductances

38
Q

What happens to A-type K+ channels expressed in the distal dendrites in the HPC? (+ref)

A

Inactivated by EPSP which locally depolarises the membrane, boosting subsequent bAPs arriving within a time window of tens of milliseconds (Magee and Johnston, 1997)

39
Q

What does the inactivation of A-type K+ channels do?

A

Facilitates the associative element of LTP

40
Q

What follows from the activation of voltage-gated Na+ channels in the distal dendrites?

A

Similar effect - enhancing the bAP and increasing influx of Ca2+ through VDCC

41
Q

What regulates the magnitude of LTP being induced at active synapses? (+ref)

A

The manipulation of dendritic conductances through non-linear interactions between the bAP and EPSP, when the EPSP precedes the bAP (Bi and Poo, 1998)

42
Q

What can the window for LTD induction be explained in terms of?

A

The interaction between the bAP

43
Q

What does the coincidence of an EPSP with the after-hyperpolarization phase of the bAP result in? (+ref)

A

A relatively small influx of Ca2+ (as seen with LFS), resulting in LTD (Caporale and Dan, 2008)

44
Q

What is another mechanism (bAP/LTD)? (+ref)

A

Inactivation of NMDA channles following the influx of Ca2+ through VDCCs, causing sublinear summation of Ca2+ signalling (Bi and Poo, 1998)

45
Q

What do mGluRs, in combination with Ca2+ influx through VDCCs lead to?

A

Activation of PLC, which can act as a signal for eCB synthesis

46
Q

What did blockade of CB1 receptors lead to? (+ref)

A

Blockade of CB1Rs by AM251 prevented LTD, indicating that retrograde eCB signaling via CB1Rs is required for LTD, through the presynaptic inhibition of neurotransmitter release (Bender, 2006)

47
Q

What does blocking the binding of BDNF to TrkBRs lead to?

A

Reduction in the synaptic response to HFS as well as the magnitude of adult hippocampal LTP

48
Q

What does blocking of binding of BDNF to TrkBRs suggest? (+ref)

A

BDNF may regulate hippocampal LTP by enhancing the synaptic response to HFS (Figurov et al., 1996)

PHOL009 (4 decks)

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