brain plasticity part 2 Flashcards
explain hebbs postualte
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)
what are the different forms of short term plasticity
faciilitation
augmentation
potentiation
deperssion
explain facilitation in 1 sentence
rapid increase in synaptic strength that occurs when 2 or motor APs invade the presynaptive terminal within milliseconds
in facilitation, if you have APs firing closer together in the presynaptic cell, what happens in the post synaptic cell
greater response on post synaptic = more facilitation (increase connection)
an the interval between stimuli / AP increases, what happens to the amount of facilitation
decreases
explain the reason behind facilitation/mechanism
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
the fact that entry of calcium into the presynaptic occurs fast after AP and the removal of Ca is slower leads to what
accumulation of calcium in presynaptic, more NT release, more facilitation/response in post synaptic neuron
increase in CA will lead to increased or decreased post synaptic activity
increased
what is the opposite process to facilitation
depression
describe depression in one sentence
sustances synaptic activity causes NT release to decrease because depleting calcium
as amount of NT increases, what happens to amount of depression
increases
what is the cause of depression
progressive depletion of pool of synaptic vesicles that are available for release
when the rate of signal increases, the vesicles deplete faster, what does that do to the strength of tramission
decreases until the pool is regeneratedw
where does short term neuropalstic occur
neuromuscular junction (neuron to neurone)
what is the time period for short term synaptic palsticn
timescale of tens of mili seconds to a few minutes
explain short term synaptic palsticity
affects the amount of NT released from presynaptic terminals in response to AP
(increase AP = increase NT release)
what is the cause of short term synaptic plastic
persistent actions of calcium ions within the presynaptic terminal
long term potentiation requires the binding of what NT to activate NMDA receptors
glutamate
long term potentiation requires the binding glutamate to activate what receptors
NMDA receptors
explain what is happening at resting potential in terms of AMPA and NMDA receptors
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)
at resting potential, what is blocking the NMDA recepto
magnums
explain what is happening during postsynaptic depolarization in terms of AMPA and NMDA receptors
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
NMDA is permeable to BLANK but blocked by magneisuum
calcium
NMDA is permeable to calcium but blocked byBLANK
magneisuum