Sodium nitroprusside-induced seizures and adenosine release in rat hippocampus

In the present study, we examined the effects of nitric oxide (NO)-related compounds, i.e. sodium nitroprusside (NO donor), diethyldithiocarbamate (NO trapper) and dithiothreitol (superoxide radical scavenger) on release of aspartate and adenosine from rat hippocampus using electrophysiological and microdialysis methods. Perfusion with 0.05 or 0.5 mM sodium nitroprusside significantly reduced high K(+)-evoked release of aspartate during high K(+) perfusion. Perfusion with 0.5 mM sodium nitroprusside always induced seizures and significantly increased release of aspartate and adenosine during washout of sodium nitroprusside. Diethyldithiocarbamate (5 mM) reversed the effects of sodium nitroprusside. Dithiothreitol (1 mM) significantly reduced the increase in adenosine release by sodium nitroprusside. These findings indicate that adenosine release is closely related to development of seizures, which are triggered by an increase in both NO itself and in part peroxynitrite, which results in reaction with superoxide radicals.