The role of postsynaptic calcium in the induction of long-term potentiation.

Abstract

Long-term potentiation (LTP), a long-lasting, activity-dependent increase in the strength of synaptic transmission, is one of the most intensively studied forms of synaptic plasticity in the mammalian brain. In the CA1 region of the hippocampus, the induction of LTP is likely to require a rise in postsynaptic calcium levels. The main source for this calcium is influx through the NMDA receptor ionophore, although other potential sources include voltage-dependent calcium channels and release from intracellular stores. Dendritic spines, the sites of synaptic contact, may function to isolate and amplify synaptically mediated increases in postsynaptic calcium. Recent evidence indicates that the magnitude of postsynaptic calcium increase is a critical variable controlling the duration of synaptic enhancement. Although a number of calcium-dependent biochemical processes have been implicated in LTP, determining their exact role remains a challenging experimental problem.