Abstracts

Nitric oxide (NO) is a free radical synthesized from L-arginine by a Ca²⁺-calmodulin-dependent NO synthase (NOS). The functional meaning of NO and NOS in epilepsy remains controversial despite previous studies from animal models. In present study, we investigated NOS expression in the hippocampus of rat with pilocarpine-induced seizures., Adult male Wistar rats (200-250g) were pretreated with atropine methylbromide (1mg/kg s.c.) and 30 min later with pilocarpine hydrochloride (330mg/kg i.p.). After 40 min, the Status epilepticus (SE) was terminated by injection of diazepam (4mg/kg i.p.). Animals were sacrificed 1 day, 3days, 2 wk (silent phase) or 1 month (chronic phase) after status. Neuronal NOS (nNOS), inducible NOS (iNOS) and epithelial NOS (eNOS) expressions and the density of mossy fiber sprouting (MFS) in the hippocampus were evaluated using immunohistochemistry and neo-Timm[apos]s histological procedures., iNOS and eNOS expressions were more strongly upregulated than nNOS expression at both phases. nNOS expression gradually increased until 3 days and decreased after 2 wk. iNOS expression had no alteration at both phases. eNOS expression tended to decrease after 2 wk. The density of MFS gradually increased and was strongest at 1 month., Our data indicate that nNOS and eNOS with the strongest upregulation in the silent phase may have a correlation with epileptogenesis while iNOS with the durability of upregulation in both phases may have something of influence on the hippocampus also after the epileptogenesis was acquired.,