Muscarinic-receptor activation stimulates oscillations in K+ and Cl- currents which are acutely dependent on extracellular Ca2+ in avian salt gland cells.

By utilizing the perforated-patch variant of the whole-cell patch-clamp recording technique, in order to maintain the integrity of the normal cellular buffering systems, we demonstrate that carbachol (CCh) stimulates simultaneous oscillations in a Ca(2+)- and voltage-activated K+ current and a linear Ca(2+)-activated Cl- current in an exocrine avian salt gland cell preparation. Similar conductance changes, although sustained rather than oscillatory, are stimulated by the Ca2+ ionophore A23187. The outward K+ current can be inhibited by tetraethylammonium chloride (TEA) whereas the Cl- current is inhibited by the Cl- channel blockers 5-nitro-2-(3-phenylpropylamino) (NPPB) and N-phenylanthranilic acid (DPC). The oscillations in current stimulated by CCh are acutely dependent on extracellular Ca2+ and are not affected by the application of low doses of caffeine. In addition, the application of caffeine at all doses fails to mimic the current transients stimulated by CCh. As both caffeine and A23187 are unable to stimulate oscillations under the perforated-patch conditions we suggest that in avian salt gland cells the primary oscillatory mechanism probably involves a one-pool mechanism of Ca2+ release which is intimately related to the activation of a Ca2+ influx pathway.