brain plasticity part 2 Flashcards

1
Q

explain hebbs postualte

A

when 2 cells are active at the same time they become assocaited so that activity in one facilitates activity in the other

(coordinated activity of a presynaptic terminal and post synaptic neuron strengths then connection between them)

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2
Q

what are the different forms of short term plasticity

A

faciilitation
augmentation
potentiation
deperssion

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3
Q

explain facilitation in 1 sentence

A

rapid increase in synaptic strength that occurs when 2 or motor APs invade the presynaptive terminal within milliseconds

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4
Q

in facilitation, if you have APs firing closer together in the presynaptic cell, what happens in the post synaptic cell

A

greater response on post synaptic = more facilitation (increase connection)

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5
Q

an the interval between stimuli / AP increases, what happens to the amount of facilitation

A

decreases

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6
Q

explain the reason behind facilitation/mechanism

A

entry of calcium into the presynaptic occurs fast after AP yet the removal of Ca is slower

=leads to accumulation of calcium, increase in NT release, increase response on post synaptic

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7
Q

the fact that entry of calcium into the presynaptic occurs fast after AP and the removal of Ca is slower leads to what

A

accumulation of calcium in presynaptic, more NT release, more facilitation/response in post synaptic neuron

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8
Q

increase in CA will lead to increased or decreased post synaptic activity

A

increased

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9
Q

what is the opposite process to facilitation

A

depression

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10
Q

describe depression in one sentence

A

sustances synaptic activity causes NT release to decrease because depleting calcium

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11
Q

as amount of NT increases, what happens to amount of depression

A

increases

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12
Q

what is the cause of depression

A

progressive depletion of pool of synaptic vesicles that are available for release

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13
Q

when the rate of signal increases, the vesicles deplete faster, what does that do to the strength of tramission

A

decreases until the pool is regeneratedw

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14
Q

where does short term neuropalstic occur

A

neuromuscular junction (neuron to neurone)

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15
Q

what is the time period for short term synaptic palsticn

A

timescale of tens of mili seconds to a few minutes

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16
Q

explain short term synaptic palsticity

A

affects the amount of NT released from presynaptic terminals in response to AP

(increase AP = increase NT release)

17
Q

what is the cause of short term synaptic plastic

A

persistent actions of calcium ions within the presynaptic terminal

18
Q

long term potentiation requires the binding of what NT to activate NMDA receptors

A

glutamate

19
Q

long term potentiation requires the binding glutamate to activate what receptors

A

NMDA receptors

20
Q

explain what is happening at resting potential in terms of AMPA and NMDA receptors

A

Glutamate binds to AMPA causing Na to enter the cell (making it more positive, but not enough for depolarization)

mg2 is blocking the NMDA receptor (therefore calcium cannot enter the cell)

21
Q

at resting potential, what is blocking the NMDA recepto

A

magnums

22
Q

explain what is happening during postsynaptic depolarization in terms of AMPA and NMDA receptors

A

when there an an increase in stimuli/firing, and there is an AP there is producing in the postsynaptic cell
=magnesium is expelled from the NMDA receptors (calcium can enter)

=leads to LTP

23
Q

NMDA is permeable to BLANK but blocked by magneisuum

A

calcium

24
Q

NMDA is permeable to calcium but blocked byBLANK

A

magneisuum

25
Q

NMDA receptor is only active when what

A

there is an AP that takes place in the post synaptic cell

26
Q

in order to activate the NMDA receptor, what does this require (think Hebbs)

A

strong coincident presynaptic and post synaptic activity (need a lot of coordinated stimuli from pre synaptic to induce AP in post)

27
Q

in LPT, after many APs are produced in post synaptic cell and there is an increase in calcium in the post synaptic cell, what happens (think membrane)

A

accumulation of ca leads to increase in membrane trafficking process

calcium will lead to more anchoring of AMPA receptors
=increases chance of more APs since we are increasing the binding sties and allowing more Na to enter)

28
Q

in LTP, when there is an accumulation of calcium in the post synaptic cell, does that lead to an increased or decreased membrane trafficking process

A

increased

29
Q

what does it mean to have an increased membrane trafficking process

A

the accumulation of CA will lead to the anchoring of more AMPA receptors

30
Q

true or false, during increased membrane tracking process, the accumulation of CA will lead to the anchoring of more NMDA receptors

A

FALSE
AMPA RECEOTORS

31
Q

explain late phase LTP

A

long term there is the activation of a protein kinase which grows a protein

=makes new dendritic spine/synapse location on the post synaptic cell
=increases communication possibility between 2 cells

32
Q

where is LTP

A

cerebral cortex, cerebellum, amygdala

33
Q

the growing and adapating quality of dendritic spines provide the basis of synaptic plasticity important for what processe

A

learning and memory

34
Q

what is the general mechanism of LTP

A

post translational modifications of existing proteins (mostly in changes of trafficking of glutamate receptors/AMPA)

35
Q

what is LTD (quickly)

A

a low frequency of stimulation causes AMPA receptors on post synaptic to internalize and disappear)

36
Q

short term memory is associated with changes in what

A

neural firing patterns dn neuromodulator/transmitter release)

37
Q

long term memory is associated with changes in what

A

assocaited with plastic changes in the brain (numbers nd strength of synapses)

38
Q
A