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
NMDA receptor is only active when what
there is an AP that takes place in the post synaptic cell
in order to activate the NMDA receptor, what does this require (think Hebbs)
strong coincident presynaptic and post synaptic activity (need a lot of coordinated stimuli from pre synaptic to induce AP in post)
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)
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)
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
increased
what does it mean to have an increased membrane trafficking process
the accumulation of CA will lead to the anchoring of more AMPA receptors
true or false, during increased membrane tracking process, the accumulation of CA will lead to the anchoring of more NMDA receptors
FALSE
AMPA RECEOTORS
explain late phase LTP
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
where is LTP
cerebral cortex, cerebellum, amygdala
the growing and adapating quality of dendritic spines provide the basis of synaptic plasticity important for what processe
learning and memory
what is the general mechanism of LTP
post translational modifications of existing proteins (mostly in changes of trafficking of glutamate receptors/AMPA)
what is LTD (quickly)
a low frequency of stimulation causes AMPA receptors on post synaptic to internalize and disappear)
short term memory is associated with changes in what
neural firing patterns dn neuromodulator/transmitter release)
long term memory is associated with changes in what
assocaited with plastic changes in the brain (numbers nd strength of synapses)
