Two components of transmitter release in retinal bipolar cells: Exocytosis and mobilization of synaptic vesicles

Ca2+-transmitter release coupling was examined using bipolar cells with large presynaptic terminals dissociated from the goldfish retina. Presynaptic Ca2+ current (I-Ca) was recorded under the whole-cell voltage clamp. Release of excitatory amino acid transmitter was simultaneously monitored as the current through N-methyl-D-asperate (NMDA) receptors of reporter cells or as the membrane capacitance (C-m) change associated with exocytosis. When I-Ca was activated by a long depolarizing pulse, a double-peaked transmitter-induced current (I-tr) was elicited in reporter cells. The rapid component of I-tr was evoked immediately after the onset of depolarization, and was affected only slightly by intracellularly applied Ca2+ chelators. The delayed slow component of I-tr was elicited during depolarization once a fixed amount of Ca2+ was accumulated in presynaptic terminals, and its appearance was suppressed or retarded by Ca-2+ chelators. Two components of transmitter release were also recognized by monitoring C-m changes elicited by the activation of I-Ca. These results suggest that bipolar cells have at least two pools of synaptic vesicles; a small, immediately releasable pool and a large releasable pool. The rapid and the delayed slow components of transmitter release may reflect exocytosis and mobilization of synaptic vesicles: respectively. (C) 1997 Elsevier Science Ireland Ltd.