Synaptic plasticity Flashcards
Why do we need synaptic plasticity?
Short term adaptation
Longer term structural changes
Learning and memory
London taxi drivers hippocampus
Larger posterior
Smaller anterior
Hippocampus is involved in spatial memory
Aplysia gill
The gill withdrawal reflex exhibits plasticity
Behavioural plasticity accompanied by synaptic modulation
Two types of synaptic plasticity
Homosynaptic, activity dependent plastic change
Heterosynpatic, modulatory input dependent plastic change
Behavioral sensitization and habituation
Plasticity occurs at the sensory neuron - motoneuron synapse
Behavioural sensitization associated with facilitation of synapse
Behavioural habituation associated with depression of synapse
5HT acts on SN which acts on MN
Heterosynaptic facilitation (addition of 5HT)
Homosynaptic depression (keep on slowly stimulating SN)
What causes changes in synaptic transmission ?
Increase in transmitter release?
Increase in sensitivity to transmitter?
A combination of both?
What causes AP to broaden in SN during Heterosynpatic facilitation
Action potential broadening occurs in the sensory neuron during heterosynaptic facilitation
This occurs because 5HT inhibits a K+ current involved in repolarization of the action potential
Repolarization of the action potential controlled by K+ channels
Broader action potential, more Ca2+ entry, more transmitter release
Effect of 5HT on transmitter release
5HT causes production of cAMP which activates PKA.
PKA phosphorylates the S-type K+ channel preventing it from opening
This broadens the action potential, and more transmitter is released
What mediates connectivity in hippocamous?
EPSP mediated by glutamate release from presynaptic neuron, activating AMPA receptors
This synaptic connectivity is highly plastic and encodes memory
Glutamate is the transmitter involved:
It acts at AMPA receptors and NMDA receptors
Key requirements for LTP
Postsynaptic depolarization (provided either by current injection or by the tetanus). A calcium influx into postsynaptic cell Activation of NMDA receptors.
3 critical features of the NMDA receptor:
Slower kinetics -window for coincidence detection, allows summation of the EPSP during the tetanus
Voltage dependent Mg2+ blockade -detection of coincidence, cell must be depolarized to unblock the NMDA channel (happens during tetanus).
Ca2+-permeability -triggering the consequences of coincidence
The sequence of events underlying LTP
Summation of synaptic currents
Depolarization
Unblocking NMDA receptor
Ca2+ influx
LTP has important postsynaptic mechanisms:
Phosphorylation of AMPA receptors
Insertion of more AMPA receptors
If activation of a synapse results in the postsynaptic neuron firing an action potential the synapse strengthens
WHY?
The NMDA receptor gives synapses in the hippocampus a quasi-Hebbian character:
Instead of the postsynaptic neuron having to fire an action potential, it needs to be depolarized sufficiently to unblock the NMDA receptor
