Regional and temporal regulation and role of somatostatin receptor subtypes in the mouse brain following systemic kainate-induced acute seizures.

Somatostatin reduces neuronal excitability via somatostatin receptors (Sst-Sst) and inhibits seizure activity. However, the expression status of the Sst subtypes in epileptic mice and their role in the antiepileptic effects of somatostatin remain unclear. Here, we show that the Sst subtypes are regulated differently by epileptic neuronal activity in mice. Systemic kainate injection rapidly and transiently elevated the Sst and Sst mRNA and reduced Sst and Sst mRNA in the hippocampus; however, among all the subtypes, only Sst mRNA was increased in the excitatory neurons of the basolateral amygdala, accompanied by a decrease in the level of Sst protein. Following kainate administration, recovery from seizure was delayed by reduced expression of Sst in the basolateral amygdala, but not in the dentate gyrus of the hippocampus; higher expression levels of Bdnf, a neuronal activity marker, were observed in both conditions. These results suggest that Sst contributes to seizure termination by feedback inhibition in the amygdala. This could be a potential therapeutic target for acute seizures.