Inhibition of the Met-enkephalin-induced K+ current in B-cluster neurons of Aplysia by nitric oxide donor.

Abstract The effects of sodium nitroprusside (SNP), a nitric oxide (NO) donor, on a methionine-enkephalin (Met-E)-induced K + current recorded from B-cluster neurons in Aplysia cerebral ganglion were investigated with voltage-clamp and pressure ejection techniques. Bath-applied SNP (10–25 μM) reduced the Met-E-induced K + current in the neurons without affecting the resting membrane conductance and holding current. The inhibitory effects of SNP were reversible. Pretreatment with methylene blue (10 μM), a non-specific inhibitor of guanylate cyclase, and hemoglobin (50 μM), a NO scavenger, decreased the SNP-induced inhibition of the Met-E-induced current. Intracellular injection of 1 mM guanosine 3′,5′-cyclic monophosphate (cGMP) or bath-applied 3-isobutyl-1-methylxanthine (IBMX; 50 μM), a nonspecific phosphodiesterase inhibitor, inhibited the Met-E-induced current. Furthermore, 1H-[1,2,4] oxadiazolo[4,3- a ]quinoxalin-1-one (ODQ, 1 μM), a more specific inhibitor of NO-stimulated guanylate cyclase, decreased the SNP-induced inhibition of the Met-E-induced current. These results suggest that SNP induces suppression of the Met-E-induced K + current recorded from B-cluster neurons of Aplysia cerebral ganglion via stimulation of cGMP formation.