Nitric oxide regulates spike frequency accommodation in nodose neurons of the rabbit.

A Ca(2+)-dependent slow spike after hyperpolarization (AHPslow) is present in about 35% of the neurons in the nodose ganglion. Although the AHPslow profoundly affects spike frequency accommodation of these neurons, the mechanisms that control the generation and the duration of the AHPslow are unclarified. N omega-Nitro-L-arginine methyl ester (L-NAME; 10 microM), a specific inhibitor of nitric oxide synthase (NOS), reduced the AHPslow by more than 92%. The L-NAME block of the AHPslow was antagonized by application of 50 microM S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide donor. The fast, Ca(2+)-dependent, spike after hyperpolarization preceding the AHPslow and the elevation of intracellular Ca2+ accompanying the AHPslow were unaffected by L-NAME treatment. These findings indicate that products of NOS activity might directly or indirectly activate the AHPslow K+ channels at a step beyond Ca2+ influx or intracellular Ca2+ mobilization.