Modulating effect of hydrogen sulfide on gamma-aminobutyric acid B receptor in recurrent febrile seizures in rats.

Hydrogen sulfide (H2S) is recognized as a new neuromodulator in regulating various brain functions. Some of our recent studies showed that H2S alleviates the hippocampal damage induced by recurrent febrile seizures (FS). In the present study, we used a rat model of recurrent FS and found that sodium sulfhydrate (NaHS, a donor of H2S) down-regulated the expression of c-fos and increased the expression of gamma-aminobutyric acid B receptor subunits 1 (GABA(B)R1) and 2 (GABA(B)R2). Hydroxylamine (an inhibitor of cystathionine b-synthase) up-regulated the expression of c-fos and down-regulated the expression of GABA(B)R2, but did not change the expression of GABA(B)R1. These results suggest that H2S plays a regulatory role through modulating GABA(B)R function in the pathogenesis of recurrent FS.