Abe K, Nakanishi K, Saito H
Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, The University of Tokyo, Japan.
Brain Res. 2000 Jan 31;854(1-2):235-8. doi: 10.1016/s0006-8993(99)02269-6.
We have recently found that intracerebroventricular (i.c.v.) administration of glutathione (GSH) inhibits pentylenetetrazol-induced convulsions in mice, suggesting that GSH has an anticonvulsive action. In the present study, we investigated whether endogenous GSH play a role in regulating seizure susceptibility, using L-buthionine-[S,R]-sulfoximine (BSO), a specific inhibitor of GSH biosynthesis. BSO treatment (3.2 micromol i.c.v. x 2, 48 and 24 h prior to experiments) decreased brain GSH level to 31.5% of control, and potentiated pentylenetetrazol-induced convulsions. Potentiation of convulsions by BSO treatment was recovered by supplying GSH (10 nmol, i.c.v.). These results suggest that endogenous GSH functions as an anticonvulsant.
