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► Med - Year 1 > Synaptic Plasticity > Flashcards

Synaptic Plasticity Flashcards

1
Q

Definition of synaptic plasticity

A

A maintained change in efficacy of a pre existing synapse and/or a change in synapse number

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2
Q

Synaptic efficacy is a function of these two factors:

A
  1. amount of presynaptic transmitter release (amount thats AVAILABLE at synapse)
  2. the responsiveness of post synaptic receptors
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3
Q

Idea that coordinated activity between pairs of cells can strengthen the connection between them and make the post synaptic cell more likely to fire based on input from pre synaptic cell

A

“Neurons that fire together wire together” -Hebbian plasticity

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4
Q

What play a critical role in human memory? What kind of memory?

A

Hippocampus-important role in encoding memories and converting short term memory into long term

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5
Q

Location of hippocampus

A

deeper parts of forebrain, in temporal lobe

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6
Q

Synaptic plasticity in the hippocampus is what type of synapse?

A

Trisynaptic circuit-3 major synapses

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7
Q

What synaptic regions in hippocampus undergo changes in synaptic strength (glutamate synapses) in response to synchronous activity?

A

between the CA3 and CA1 regions. highly studied and useful for experimental approaches

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8
Q

A maintained change (increased size) in post synaptic response

A

Long term potentiation (LTP)

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9
Q

A measure of plasticity is a change in

A

EPSP

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10
Q

Coincidence detector

A

NMDA. can sense glutamate release in presynaptic cell and the depolarization in post synaptic cell

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11
Q

What are the two critical features to detect when pre and post synaptic cells are active at same time?

A

Glutamate release of pre synaptic and depolarization of post synaptic

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12
Q

What allows long term changes of efficacy to produce LTP?

A

Calcium influx through NMDA channel

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13
Q

If presynaptic neuron fires at high level, it will release glutamate and stimulate what receptor?

A

AMPA receptors

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14
Q

What causes a much stronger depolarization after glutamate release stimulates AMPA receptors?

A

AMPA stimultion —> Temporal summation —> Strong depolarization

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15
Q

How do NMDA receptors get activated to trigger synaptic plasticity? (2)

A

High frequency synaptic activity and back propagating action potnetials in dendrites + synaptic glutamate release

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16
Q

What in dendrites support the active propagation of action potential into the dendritic tree?

A

Voltage-gated sodium channels (same ones that trigger AP in axon, but not nearly same density)

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17
Q

The back propagating AP can spread

A

depolarization

18
Q

LTP results in increased number of what?

A

post synaptic AMPA receptors (one example of that kinds of things that can happen-target different parts of pre synaptic apparatus or post synaptic receptor)

changes in amount of transmitter release

19
Q

Increase in AMPA receptors will cause

A

increase in synaptic strength

20
Q

Plausible mechanism of how calcium affects trafficking of AMPA receptors

A

Ca influx through NMDA receptor –> activates Ca2+/calmodulin kinase II or PKA —> substrate phosphorylation–> less internalization of AMPA receptors, move to membrane.

kinase activity eventually stop. short term effect

21
Q

2 important effects of LTP

A
  1. can alter size and shape of synapse

2. cause growth of new synapses

22
Q

Short term plasticity

A

regulation of signaling proteins (kinases etc)

23
Q

Long term plasticity

A

transcriptional regulators and growth of new synapses

24
Q

CREB

A

involved in transcriptional regulators for synapse growth proteins (long term plasticity)

25
Q

Mechanisms for decrease synaptic strength when activity is not synchronous

A

long term depression (LTD)

26
Q

LTD

A

activity induced decrease in synaptic strength

27
Q

decrease in size of EPSP

A

LTD

28
Q

LTD can be due to these two factors:

A
  1. decreased number of post synaptic AMPA receptors

2. changes in transmitter release

29
Q

How does calcium influx affect LTD?

A

can affect phosphoryation such that you see increases the internalization of AMPA receptors

Ca2+–>protein phosphatase –> dephosphorylate substrate –> internalization of AMPA receptors

30
Q

These can act on CB1 receptors, shown to be involved in many LTD forms

A

endocannabinoids

31
Q

Post synaptic activity induces release of this signal that alters presynaptic release

A

retrograde signal

32
Q

What might trigger endocannabinoid release from post synaptic cell?

A

Calcium influx in Ca2+ channel, or glutamate receptors that are coupled to G proteins (mGluR)

33
Q

Epilepsy

A

disruptive function (seizure) due to overly excitatory connections, fire at high frequencies

34
Q

Activity of this part of the hippocampal formation that is thought to contribute to the formation of new episodic memories. Its nerons receive the hippocampals formation’s major excitatory input from cortex

A

Dentate gyrus

35
Q

Form of synaptic reorganization in the dentate gyrus that occurs in epilepsy.

A

Mossy fiber sprouting

36
Q

The axons of dentate gyrus granule cells

A

mossy fibers

37
Q

Effects of mossy fiber sprouting

A

formation of new synaptic connections and growth of them that can occur as result of seizure

38
Q

Kindling

A

Development of seizures and epilepsy. Circuit now has maintained change in excitability, more likely to become excitable and cause subsequent seizures= Lowers threshold for subsequent seizures.

39
Q

Amount of dendritic spins in Fragile X compared to WT

A

many more

40
Q

Amount of dendritic spines in Rett Syndrome compared to wildtype

A

decrease number of spines in synapses

41
Q

New research for developmental brain disorders

A

used to think it was permanent brain abnormalities. now see that it may result from disruptions at trillions of synapses between brain cells. potentially reversible disruptions

► Med - Year 1 (48 decks)

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