Re-evaluation of calcium currents in pre- and postsynaptic neurones 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 microM 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 (omega CgTX) suppressed a large fraction of the Ba2+ current irreversibly. About 10% of the Ba2+ current was resistant to both DHPs and omega CgTX. 6. The omega CgTX-sensitive component was not sensitive to changes in the holding potential between -120 and -50 mV. The omega CgTX-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 microM Cd2+ completely abolished the Ca2+ current. 9. About 25% of the Ba2+ currents were blocked by nifedipine (10 microM) in ciliary cells. The nifedipine-resistant component was partly blocked by omega CdTX (10 microM) leaving a small component (about 20%) which was resistant to both nifedipine and omega CgTX. 10. In ciliary cells, the fraction of Ba2+ currents blocked by omega CgTX was not affected by the presence or absence of nifedipine. Similarly, nifedipine blocked the Ba2+ currents to the same extent whether omega CgTX 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 omega CgTX and membrane potential.
Yawo
H
H
Department of Physiology, Kyoto University Faculty of Medicine, Japan.
Momiyama
A
A
D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000818:Animals; D001464:Barium / Q000378:metabolism; D015220:Calcium Channels / Q000187:drug effects; D000252:Calcium-Transporting ATPases / Q000187:drug effects / Q000502:physiology*; D002642:Chick Embryo; D002924:Ciliary Body / Q000166:cytology / Q000378:metabolism*; D004095:Dihydropyridines / Q000494:pharmacology; D016623:Ion Pumps / Q000187:drug effects; D007477:Ions; D008564:Membrane Potentials / Q000502:physiology; D008978:Mollusk Venoms / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology; D012583:Schwann Cells / Q000187:drug effects; D013569:Synapses / Q000378:metabolism* / Q000648:ultrastructure; D020866:omega-Conotoxin GVIA
D015220:Calcium Channels; D004095:Dihydropyridines; D016623:Ion Pumps; D007477:Ions; D008978:Mollusk Venoms; D001464:Barium; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D020866:omega-Conotoxin GVIA; D000252:Calcium-Transporting ATPases; D009543:Nifedipine