Synaptic Plasticity Flashcards
Synaptic Plasticity is
the ability to reorganise by creating new neural pathways to adapt
Mechanisms of synaptic plasticity could include:
- altering the amount of
neurotransmitter released - changing the no. receptors post-
synaptically - changing signaling molecules inside
neuron - changing gene transcription
Synaptic efficacy/strength changes with —–, many of these changes are ——- dependent
- time
- activity
Learning:
involves adaptive changes in synaptic connectivity which will in turn alter behaviour
Hebb’s Rule:
synapses can change conformation depending on how active or inactive it is
Hebb’s Cell Assembly:
internal representation of an object consists of the cortical cells that are activated by it - cell assembly - cells were reciprocally interconnected
Hebb’s cell assembly hypothesis:
- activation of the cell assembly
persisted long enough leading to
consolidation/growth process - reciprocal connection would be more
effective; fire together and wire
together - subsequently, if only a fraction of
assembly cells were activated by a
later stimulus, the strengthened
connections could cause the whole
assembly to activate
Rules of Synaptic Modification:
- fire together wire together
- fire out of sync lose their link
- individual stimulation may be
insufficient to fire an action potential - summation of two signals is
acceptable
Connectome:
- system of neural pathways in a brain
or nervous system considered
collectively
Long-Term Potentiation:
- mechanism underlying synaptic
strengthening - describes a phenomenon whereby
high frequency stimulation of a
neurone leads to increased EPSP to a
subsequent single stimulus pulse - long-term changes in expression of
genes and turnover of peptides
undelry this phenomenon = a form
of plasticity
An example of long term potentiation is
high frequency electrical stimulation of the perforant pathway
Excitatory postsynaptic potential can last hours
Cellular Physiology of LTP:
- Glutamate release onto membrane
at resting potential - AMPA receptor activated to create
EPSP - NMDA receptor blocked by Mg2+
- depolarisation from AMPA activation
not sufficient to expel Mg2+ - Glutamate release continued onto
active (depolarised) cell - AMPA receptor activated
- Mg2+ block on NMDA removed
- Na+ enters through AMPA and
NMDA channels - Ca2+ through NMDA receptors
- leads to the activation of protein
kinase C, CaMKII (Calcium
calmodulin-dependent protein
kinase II)
1)phosphorylates existing AMP
receptors increasing their
effectiveness
2) stimulates the insertion of new
AMPA receptors into the membrane
CaMKII Molecular Switch:
- has autocatalytic activity so becomes
phosphorylated - constitutively active; no longer
requires Ca2+ - maintains phosphorylation, insertion
of AMPA after depolarising stimulus
has receded - molecular switch which maintains
increased excitability of neuron for
minutes to hours
Early Phase Long-term potentiation:
- a minute to an hour
- explained by the actions of Ca2+ and
the subsequent enhancement of
AMPA receptors, presynaptic events
etc
Late Phase Long-Term Potentiation:
- hours, days, months
- requires new protein synthesis
- can involve morphological changes
and new synapses - Ca2+ activated signal transduction
Before and after of what?
LTP and Pre-synaptic Neuron:
Long Term Depression
