Inhibition of high K(+)-evoked gamma-aminobutyric acid release by sodium nitroprusside in rat hippocampus.

摘要

To clarify whether nitric oxide (NO) modifies high K(+)-evoked gamma-aminobutyric acid (GABA) release, we examined the effects of sodium nitroprusside, an NO donor; diethyldithiocarbamate, an NO trapper; dithiothreitol, a superoxide radical scavenger; and 1H-(1,2,4)oxadiazole(4,3-a)quinoxalin-1-one, a specific guanylyl cyclase inhibitor, on high (100 mM) K(+)-evoked GABA release from rat hippocampus in vivo using microdialysis. Perfusion with 0.5 or 5 mM sodium nitroprusside significantly reduced high K(+)-evoked GABA release. Co-perfusion with 0.5 mM sodium nitroprusside and 5 mM diethyldithiocarbamate or 0.5 mM 1H-(1,2,4)oxadiazole(4,3-a)quinoxalin-1-one significantly enhanced high K(+)-evoked GABA release. Co-perfusion with 0.5 mM sodium nitroprusside and 1 mM dithiothreitol tended to increase it. These results demonstrate that sodium nitroprusside reduces high K(+)-evoked GABA release both via an NO/cyclic GMP-dependent pathway and via an NO-dependent, but cyclic GMP-independent, pathway in rat hippocampus in vivo.