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NSB Lectures > Synaptic Plasticity > Flashcards

Synaptic Plasticity Flashcards

1
Q

What is synaptic plasticity?

A

The ability of the brain to adapt by creating new neural pathways.

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2
Q

The change of synaptic efficiency and strength depends on what?

A

The activity of the pre and post-synaptic neuron.

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3
Q

Which ‘rule’ determined that synapses could change due to how active or inactive they are?

A

Hebbs’ rule

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4
Q

For Hebb’s rule, what type of activity will induce a lasting cellular change that adds to its stability?

A

A persistent or repetitive activity.

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5
Q

Neurons that ____ together, ____ together.

A

Fire
Wire

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6
Q

Neurons that fire out of ____, lose their ____.

A

Sync
Link

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7
Q

Hebb’s cell assembly hypothesis proposed a ____ activation of the cell assembly would cause a growth process.

A

Long

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8
Q

For Hebb’s cell assembly hypothesis, after a growth process has been created, if a fraction of the cells of the assembly were activated by a later stimulus, what would happen to the assembly?

A

As the growth process has strengthened the connections, a fraction of cells activated in the assembly could cause the whole assembly to be activated.

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9
Q

What can increase the chances of creating an excitatory postsynaptic potential, great enough to fire an AP?

A

Having two stimulus’ of the same object e.g. seeing and smelling something at the same time.

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10
Q

Repeated association of two synapses from their stimulation, can strengthen the synapse. What would happen if one of the synapse was activated, without the other?

A

The synapse on it’s own would be sufficient enough to create an excitatory postsynaptic potential, and elicit an AP.

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11
Q

What is the collective system of neural pathways/structural connectivity in a brain or nervous system known as?

A

Connectome
‘Wiring diagram’
Can include Synaptome + Epigenome.

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12
Q

What is learning the relevant molecular states at each synaptic connection called?

A

Synaptome

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13
Q

What is learning the relevant changes in the nucleus of each neuron called?

A

Epigenome

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14
Q

Which significant mechanism that occurs in the hippocampus and cerebral cortex, underlies synaptic strengthening, and is centrally important in processes of learning and memory?

A

Long term potentiation.

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15
Q

If there is a high frequency stimulation of a neuron, what does this do to the amplitude of an excitatory post synaptic potential?

A

Increases the potential.

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16
Q

How long would a long term potentiation last, if there is high frequency electrical stimulation?

A

Hours

17
Q

How long would a long term potentiation last, if there are multiple high frequency electrical stimulations?

A

Days or months.

18
Q

What two receptors are important for long term potentiation?

A

AMPA
NMDA

19
Q

Describe the cellular physiology of long term potentiation.

A

Glutamate released onto inactive cell.
AMPA receptor activated to create excitatory post synaptic potential.
NMDA receptor blocked by Mg2+ (depolarisation from AMPA activation not sufficient to expel this).
Glutamate released onto active cell (membrane depolarised).
AMPA receptor activated.
Mg2+ block on NMDA relieved.
Na+ goes through AMPA + NMDA channels.
Ca2+ goes through NMDA receptors.

20
Q

Calcium entry through NMDA receptors leads to the activation of what?

A

Protein kinase C
CaMKII

21
Q

Protein Kinase C and CaMKII are activated by Ca2+ passing through NMDA receptors. What do these kinases do to AMPA?

A

Phosphorylates existing AMPA receptors, increasing their effectiveness.
Stimulates insertion of new AMPA receptors into the membrane.

22
Q

What is the CaMKII molecular switch?

A

Maintains increased excitability of neurons as CaMKII has an autocatalytic activity and can phosphorylase itself. It therefore no longer needs Calcium and is able to maintain this phosphorylation + the insertion of AMPA receptors, after the depolarising stimulus has receded.

23
Q

What is the difference between early and late phase long term potentiation?

A

Early - lasts <1hr. Caused by Ca2+ + the enhancement of AMPA receptors.
Late - >months. Needs new protein synthesis. There can be morphological changes and new synapses. There is also Ca2+ activated signal transduction.

24
Q

How is long term potentiation involved in presynaptic events?

A

Postsynaptic neuron can feedback to the presynaptic via Nitric Oxide, resulting in increased glutamate release.

25
Q

The overload of which ion is essential in exitotoxicity?

A

Calcium

26
Q

Low frequency stimulation is linked to what condition?

A

Long term depression.

27
Q

What does a low frequency stimulation do to the amplitude of an excitatory post synaptic potential?

A

Decreases its amplitude.

28
Q

What happens to AMPA receptors when there is a low level stimulation?

A

They get de-phosphorylated and removed from the membrane.

29
Q

What do prolonged low level rises in Ca2+ activate?

A

Phosphatases.

30
Q

____ receptor activity in the hippocampus is essential for both long term potentiation and ____ learning.

A

NMDA
Spatial

31
Q

Which receptor antagonist has been proven to block hippocampal long term potentiation and blocked learning in the Morris water maze?

A

AP5-NMDA receptor antagonist.

32
Q

How does alcohol affect NMDA and memory?

A

Alcohol is an NMDA antagonist and blocks the normal long term potentiation process.

33
Q

Which drug class are modulators of GABA a receptors + can lead to anterograde amnesia?

A

Benzodiazepines.

34
Q

Which neurotransmitter has a role in memory and learning?

A

ACh

35
Q

Scopolamine impairs spatial learning. What type of drug is this?

A

Muscarinic antagonist.

36
Q

What type of inhibitors are commonly used in Alzheimers?

A

Acetylcholinesterase

37
Q

How can long-term morphine or diamorphine use cause abnormal synaptic plasticity?

A

Can cause a reduced sensitivity to u-opoid receptors.

38
Q

How does smoking show up as abnormal synaptic plasticity?

A

Nicotine binds to nicotinic receptors. Smoking increases the numbers of specific nicotinic receptor subunits in the brains of smokers.

NSB Lectures (48 decks)

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