| Abstract: | Experiments on isolated neurons of the molluskPlanorbarius corneus under membrane voltage clamp conditions showed that furosemide (2×10?4 to 1×10?3 g/mg) inhibits the increase in chloride conductance evoked by iontophoretic application of acetylcholine, suberyldicholine, and gamma-aminobutyric acid (GABA). If microelectrodes filled with potassium sulfate were used in the experiments furosemide did not shift the reversal potential, but when microelectrodes filled with potassium chloride were used the reversal potential of the chloride-dependent responses became less negative. In the last case, the action of furosemide evidently was exhibited not only on passive chloride conductance of the chemoreceptive membrane, but also on active chloride transport. Furosemide had no effect on sodium- and potassium-dependent responses evoked by activation of choline receptors. Unlike D-tubocurarine, which selectively blocks acetylcholine effects, furosemide also depressed conductance evoked by GABA. In the presence of furosemide chloride-dependent responses not only were reduced in amplitude, but also developed more slowly. It is postulated that the action of furosemide is aimed not at receptors, but at chloride channels of the chemoreceptive membrane common to both acetylcholine and GABA. |
