| Abstract: | The present study was undertaken to assess the effects of sodium nitroprusside (SNP) and diethylamine NO(C2H5)2NN(O)NO]?Na+ (DEA/NO), NO donors, on an acetylcholine (ACh)-induced Cl? current in identified Onchidium neurons using voltage-clamp and pressure ejection techniques. Bath-applied SNP (10 μM) and DEA/NO (5–10 μM) reduced the ACh-induced Cl? current in the neurons without affecting the resting membrane conductance and holding current. The suppressing effects of NO donors were concentration-dependent and completely reversible. Pretreatment with 1H-1,2,4]oxadiazolo-4,3-a]quinoxalin-1-one (1 μM), a specific inhibitor of NO-stimulated guanylate cyclase, and hemoglobin (50 μM), a nitric oxide scavenger, decreased the SNP-induced inhibition of the ACh-induced current. Intracellular injection of guanosine 3′,5′-cyclic monophosphate (cGMP) or bath-application of 3-isobutyl-1-methylxanthine (50 μM), a non-specific phosphodiesterase inhibitor, inhibited the ACh-induced current, mimicking the effect of NO donors. These results suggest that SNP and DEA/NO inhibit the ACh-induced Cl? current and that this effect is mediated by an increase in intracellular cGMP. © 1998 John Wiley & Sons, Inc. J Neurobiol 35: 388–394, 1998 |
