Neural Plasticity
Perhaps the brain's greatest asset is its ability to learn and store experiences and events.
Memory is the ability to store and recall learned changes.
Short-term synaptic plasicity usually involves presynaptic changes.
Potentiation
Facilitation is a short term increase in strength lasting only milliseconds, while potentiation lasts tens of seconds to several minutes, outlasting the period of high-freqency stimulation. In general, longer-lasting modifications require longer periods of stimulation.
Three potential explanations may be behind potentiation, with the first most often true
- more neurotransmitter may be released, usually due to increased Ca2+ influx
- postsynaptic receptors may become more responsive in number or sensitivity
- both mechanisms may be acting
Long term potentiation
Long term potentiation, or LTP, can be generated by high frequency stimulation. LTPs are easily seen in the CA1 region of the hippocampus, a part of the cortex long associated with memory formation.
LTPs are input specific, meaning only the previously involved pre-synaptic neuron's synapses will induce increased EPSPs. They also require concurrent postsynaptic depolarization for LTP to form.
What this means is LTP is best induced by cooperativity, where enough presynaptic inputs must fire at the same time. In this way, weak synaptic inputs can become associated with each other and remain so thereafter.
Cells in the CA1 region of the hippocampus use glutamate, with both AMPA and NMDA receptors activated. LTP requires increases in postsynaptic Ca2+, mediated by NMDA channels. Ca2+ then goes on to activate protein kinase C and calcium-calmodulin dependent kinase, through from this point on how LTPs remain is obscure.
Habituation
Habituation is a decrease in synaptic strength following a period of increased firing. At least some of the time, habituation results from decreased levels of neurotransmitter being released, again demonstrating the importance of presynaptic changes in synaptic plasticity.
Long term depression
Long term depression can occur in the Purkinje cells in the cerebellum. Purkinje cells use inhibitory GABA as a neurotransmitter and represent the only output from the cerebellar cortex. Each Purkinje cell receives powerful excitatory contact from climbing fibres from the inferior olive and from about 150,000 parallel fibres from tiny granule cells.
Parallel fibre synapses lose strength when they are active in parallel with climbing fibre activation. This happens primarily through reduction of post-synaptic AMPA glutamate channels.
Long term potentiation can also occur in Purkinje cells, through mechanisms involving the presynaptic terminal.