The role of nitric oxide in genetic model of absence epilepsy in rats

Abstract

Involvement of nitric oxide (NO) in the regulation of the epileptic activity was studied in WAG/Rij rats, a genetic model of absence epilepsy. I.c.v. administration of NO donors: S-nitroso-N-acetylpenicillamine (SNAP, 0.5 and 5 μg), 3-morpholino-sydnonimine (SIN-1, 0.5 and 5 μg) or sodium nitroprusside (SNP, 2 and 20 μg) enhanced namber of spike wave discharges (SWD) after the higher dose and had no effect on the mean duration of SWD. On the other hand, i.c.v. administration of NO synthase inhibitors, L-NG-Nitro-arginine (NARG, 20, 200μg) or L-NG-Nitro-arginine methyl ester (L-NAME, 20, 100 μg) dose-dependently decreased the number of SWD. None of the NO synthase inhibitors affected mean duration of SWD. In contrast to i.c.v., the peripheral administration of L-NAME (7.5 −60 mg/kg i.p.) increased the number of SWD and had no effects on their duration. These results suggest that NO synthetized in the central nervous system promotes absence seizures in WAG/Rij rats, however peripheral administration of L-NAME aggravates absence epilepsy.