ABSTRACT
Arrival of a nerve impulse at a nerve terminal leads to opening of voltage-gated calcium (Ca2+) channels and rapid influx of Ca2+. The increase in Ca2+ concentration at the active zone from a basal level of 100 nM to more than 200 µM triggers the fusion of docked synaptic vesicles, resulting in neurotransmitter secretion (Barrett and Stevens, 1972; Llinás et al., 1981, 1992; Augustine and Neher, 1992; Zucker, 1993; Heidelberger et al., 1994). Subsequent increase in cytosolic Ca2+ concentration may promote trafficking of synaptic vesicles (Llinás et al., 1991; Rosahl et al., 1995; Pieribone et al., 1995) regulated by cytoskeletons such as F-actin (Bahler and Greengard, 1987; Trifaró and Vitale, 1993). A considerable number of molecular mechanisms have been implicated in the cascade of protein-protein interaction leading from Ca2+ influx to exocytosis and synaptic vesicle recycling (Südhof and Jahn, 1991; Bennett and Scheller, 1994; Rothman, 1994; Südhof, 1995; De Camilli andTakei, 1996).
