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Long Term Potentiation in Vertebrates
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(Memory & Learning) Biological Mapa Mental sobre Long Term Potentiation in Vertebrates, creado por n.c.wetmore el 26/04/2013.
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biological
memory & learning
biological
memory & learning
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n.c.wetmore
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Long Term Potentiation in Vertebrates
Long-Term Potentiation (LTP)
one+ axons connected to dendrite bombard it with rapid series of stimuli
burst of intense stimulation leaves some of the synapses potentiated for minutes, days or weeks
Specificity
if some of synapses onto cell have been highly active and others haven't, only active ones become strengthened
cooperativity
nearly simultaneous stimulation by two+ axons produces LTP more strongly than repeated stimulation by just one axon
Associativity
pairing weak input with strong input enhances later response to weak input.
LTP matches what we would expect of Hebbian synapses
Synapse that was almost completely inactive before LTP becomes effective afterward
Kerchner & Nicoll (2008)
Long-term depression (LTD)
prolonged decrease in response at a synapse, occurs for axons that have been less active than others
compensatory process
as one synapse strengthens, another weakens
Royer & Pare (2003)
AMPA and NMDA Synapses
in few cases, LTP depends on GABA synapses
in most it depends on changes in glutamate synapses
brain has several receptors for glutamate
NT identify diff dopamine receptors by number and diff GABA receptors by letter
for glutamate, named different receptors after certain drugs that stimulate them
AMPA receptor excited by NT glutamate but can respond to drug called AMPA
NMDA receptor also ordinarily excited only by glutamate but can respond to drug called NMDA
both are ionotropic receptors
when they are stimulated they open a channel to let ions enter the postsynaptic cell
AMPS receptor typical ion tropic receptor opens sodium channels
NMDA receptor is diff: response to transmitter glutamate depends on degree of polarisation across the membrane
when glutamate attaches to NMDA receptor while membrane is at resting potential, ion channel is blocked by magnesium ions
NMDA channel opens only if magnesium leaves and surest way to detach magnesium is to depolarise membrane, decreasing negative charge that attracts it
Presynaptic Changes
LTP depends on changes in the presynaptic neurone instead or in addition
Extensive stimulation of postsynaptic cell causes it to release a retrograde transmitter that travels back to presynaptic cell to modify it
in many cases, retrograde transmitter is nitric oxide
As a result, presynaptic neurone decreases its threshold for producing at ion potentials
increases release of NT
expands its axon
releases its transmitter from additional sites along its axon
LTP reflects increased activity by the presynaptic neurone as well as increase responsiveness by the post-synaptic neurone
Consolidation Revisted
LTP in hippo is important for certain types of learning
as time passes and learning proceeds, memory become less dependent on hippo and more on cerebral cortex
gradual over varying periods of time
fMRI showed after people learned some associations they showed more activity in hippo after 15 min
and more in cerebral cortes after 24 hours
Takashima et al (2009)
we demonstrate a shift to cerebral cortex both over period of one day and many years
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