T1L19 synaptic plasticity Flashcards
learning def
learning is the response of the brain to environmental events and involves adaptive changes in synaptic connectivity which will in turn alter behaviour
flow chart of neurons in memory
group of connected neurons:
external stimulus
>
activation of cell assembly
>
reverberating activation even after stimulus removed
>
Hebbian modification strengthens reciprocal connections between neurons that are active at the same time
>
the strengthened connections of the cell assembly contain the engram for the stimulus
>
after these events, partial activation of the cell assembly leads to activation of the whole thing, representing the stimulus
hebbs rule
Neurons that fire together wire together
Neurons that fire out of sync lose their link.
strengthening and weakening transmissions in brain provide means by which learning occurs
long term potentiation LTP
part of brain and 3 kinds
hippocampus- shape means that pathways can be easily distinguished
high frequency stimulation (HFS) of the perforant pathway»_space;higher EPSP amplitude (lasts days/months)
temporal: summation of inputs reaches a stimulus threshold that leads to the induction of an LTP eg repetitive HFS
associative: simultaneous stimulation of strong and weak pathways will induce LTP at both pathways (spatial stimulation)- cells that fire together wire together
specific: LTP at one synapse is not propagated to adjacent synapses (input specific)
a nice way to remember
Cell A – sensory input for sight of rose
Cell B – sensory input for smell of rose
Cell C – sensory input for smell of onion
Individually stimulation of the hippocampal neuron by any of these cells may be insufficent to create an EPSP great enough to fire an action potential
When A and B are activated together – on seeing and smelling the rose
the coincident EPSPs may summate sufficiently to cause an action potential in the hippocampal neuron
If this association is made repeatedly - the simultaneous firing of cells A and B onto the hippocampal neuron - those synapses will be strengthened
(over the synapse from cell C which does not fire coincidently).
The strengthening of the synapses of cell A and B will be sufficient that they will individually be able to elicit action potentials in the hippocampal neuron.
->The sight of a rose will become associated with the smell of a rose rather than the smell of an onion.
LTP what happens at the synapse
glutamate release into inactive cell (ie resting potential)
- AMPA receptor activated to create EPSP
- NMDA receptor blocked by Mg2+
- depolarization from AMPA not sufficient to expel mg2+
glutamate released into active celll (ie depolarized)
- AMPA activated
- Mg2+ comes through NMDA receptor
- Na+ comes through AMPA and NMDA
- Ca2+ through NMDA
ca2+ activates protein kinase C and CaMKII
this increases AMPA receptor effectiveness and stimulates new AMPA receptor in membrane
more AMPA receptor > bigger EPSP
CaMKII
- sustained activity after repolarization
- activated by ca2+ through NMDA
- autocatalytic (phosphorylates itself)- this activates it so calcium is no longer needed
inserts AMPA receptors
sustained for hours (increase neuron excitability)
presynaptic events in LTP
- postsynaptic feedback by retrograde transmitter NO
- NO activates guanylyl cyclase in presynaptic terminal
- this makes 2ndry messenger cGMP
- leads to increase glutamate release from synapse
late phase LTP
- protein synthesis required
- protein synthesis inhibitors prevent long term memories
early vs late phase LTP
early phase > minutes to hours. sustained by CaMKII
late phase> hours/days/months
- requires protein synthesis
-
ca2+ activates signal cascades:
- activates new protein synthesis from local mRNAs
- filter back to cell body to stimulate new gene transmission, proteins recruited to synapse
long term depression LTD
LTP caused by high frequency stimulation
LTD caused by low frequency stimulation causes opposite (decrease EPSP)
- NMDA dependant
- AMPA receptors dephosphorylated and removed
- prolonged low levels of Ca2+ activate phosphatases rather than kinases
rats stufy
those with blocked NMDA receptors stop rats from learning
drug effects on learning and mems
alcohol- NMDA receptor antagonist (blackouts)
benzodiazepines- indirect GABAa agonist
- increases affinity for GABA
- more channel openings
cholinergics/anticholinergics
- acetylcholinergic system reaches hippocampus
- muscarinic receptor antagonist suppresses theta waves and impairs visual learning
alzheimers- acetylcholinesterate inhibitors improve memory
( may also improve attention in healthy brain)
