Although numerous biochemical and electrophysiological studies have already established many of the properties of the putative Ca2+ receptor for exocytosis at the synapse, the molecular mechanism that involves the influx of Ca2+ and the release of neurotransmitters has remained elusive. Several relationships have been established between neurotransmitter release and Ca2+ channel involved, but no work attempting to connect a particular neurotransmitter release, the effector which produces the release and the opening of a Ca2+ channel type has been performed. This work shows, data dealing with this subject. Based on our results, we have reached the following conclusions: (1) Ca2+ channel types P/Q, N and L mediate Ca2+ entry evoked by high KCl and veratridine, and P/Q and N but not L-type Ca2+ channels are involved when the effector is 4-aminopyridine (4-AP); (2) When we compare the relationship between the amino acid release and the Ca2+ channels which are opened by different depolarizing agents, we find that the release of a particular amino acid neurotransmitter not only depends on the opening of the voltage-dependent Ca2+ channel but also on the effector which produces the opening; and (3) the amount of amino acid release evoked by the different depolarizing agents is not correlated with the elevation of intracellular Ca2+ produced by them. From all of these results, we may conclude that calcium concentration in the active zone is not the only important factor in mediating amino acid release.