Abstract
Long term potentiation (LTP) is a widely studied form of synaptic plasticity. Brief tetanic stimulation of synaptic afferents in several areas of the brain, most notably the hippocampus, produces long lasting changes in the synaptic strength. The induction of LTP requires in the limit a significant activation of the NMDA receptor and the subsequent entry of calcium into the post synaptic cell. The maintenance of LTP requires at least in part a change in presynaptic function. This review addresses the current thinking in the literature on how a post synaptic induction event may be communicated to the presynaptic terminal and subsequently lead to a series of poorly defined biochemical process that ultimately lead to an enhancement in the efficiency of the potentiated terminal.
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