REEVALUATION OF CALCIUM CURRENTS IN PRESYNAPTIC AND POSTSYNAPTIC NEURONS OF THE CHICK CILIARY GANGLION

1. Presynaptic nerve terminals of ciliary ganglia of the chick embryo were identified by the accumulation of dextran-tetramethylrhodamine applied to the cut end of the oculomotor nerve. Ca2+ currents were then recorded from the identified nerve terminals. 2. Whole-cell recordings were carried out simultaneously from a presynaptic terminal and its postsynaptic cell. The generation of presynaptic Ca2+ currents induced a postsynaptic response with a short delay. Electrical coupling was present in eight of fifteen pairs. The coupling ratio did not exceed 5%. 3. High-threshold Ba2+ currents were observed in presynaptic terminals without any evidence for the presence of low-threshold Ca2+ channels. The Ba2+ current was completely blocked by 50 muM Cd2+. 4. The presynaptic Ca2+ current induced by a long depolarizing pulse showed inactivation, but this inactivation was diminished when Ca2+ was replaced with Ba2+. 5. The presynaptic Ba2+ current was insensitive to dihydropyridines (DHPs). Omega-Conotoxin GVIA (omegaCgTX) suppressed a large fraction of the Ba2+ current irreversibly. About 10% of the Ba2+ current was resistant to both DHPs and omegaCgTX. 6. The omegaCgTX-sensitive component was not sensitive to changes in the holding potential between - 120 and - 50 mV. The omegaCgTX-resistant component tended to be inactivated at depolarized holding potentials. 7. In some perisynaptic Schwann cells, small Ca2+ currents were observed. These Ca2+ currents increased monotonically with depolarization. 8. Only high-threshold Ca2+ channel currents were observed in postsynaptic ciliary cells. Exposure to 50 muM Cd2+ completely abolished the Ca2+ current. 9. About 25 % of the Ba2+ currents were blocked by nifedipine (10 muM) in ciliary cells. The nifedipine-resistant component was partly blocked by omegaCgTX (10 muM) leaving a small component (about 20 %) which was resistant to both nifedipine and omegaCgTX. 10. In ciliary cells, the fraction of Ba2+ currents blocked by omegaCgTX was not affected by the presence or absence of nifedipine. Similarly, nifedipine blocked the Ba2+ currents to the same extent whether omegaCgTX was present or not. The Ba2+ currents potentiated by Bay K 8644 were eliminated by nifedipine. 11. It is concluded that the presynaptic terminal of chick ciliary ganglion did not possess DHP sensitive Ca2+ channels in contrast with the postsynaptic cell. Two subpopulations of presynaptic Ca2+ channels were distinguishable by their sensitivity to omegaCgTX and membrane potential.