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Zentrum der Physiologie, Klinikum der Johann Wolfgang Goethe-Universität, Frankfurt am Main, Germany.

1. Membrane voltage (Vm) recordings were obtained from isolated rat pinealocytes using the patch-clamp technique. In parallel to the electrophysiological experiments, intracellular Ca2+ measurements were performed using fura-2. 2. The resting Vm averaged -43 mV and replacement of extracellular NaCl by KCl completely depolarized the cells. This indicates that the resting Vm is dominated by a K+ conductance. Single-channel recordings revealed the presence of a large conductance Ca(2+)-activated charybdotoxin-sensitive K+ channel. 3. Application of ACh (100 microM) depolarized the pinealocytes on average by 16 mV. The depolarizing effect of ACh was mimicked by nicotine (50 microM) and was prevented by tubocurarine (100 microM). 4. The ACh-induced depolarization was largely abolished in the absence of extracellular Na+, but was not significantly affected by extracellular Ca2+ removal. 5. Application of ACh (100 microM) caused an increase in [Ca2+]i. This increase was completely dependent on the presence of extracellular Ca2+ and was largely reduced after extracellular Na+ removal. Nifedipine (1 microM) reduced the ACh-induced increase in [Ca2+]i by about 50%. 6. Our findings indicate that in rat pinealocytes stimulation of a nicotinic ACh receptor (nAChR) induces depolarization mainly by Na+ influx via the nAChR. The depolarization then activates L-type Ca2+ channels, which are responsible for the nifedipine-sensitive portion of the intracellular Ca2+ increase. Ca2+ influx via the nAChR probably also contributes to the observed rise in [Ca2+]i.