Suppression by sodium valproate of gamma-vinyl GABA-induced facilitation of visual evoked potentials in rats

A single dose (500 mg/kg, i.p.) of GABA-transaminase inhibitor, gamma-vinyl GABA (GVG), administered to Wistar rats caused time-related 2--3-fold enhancement of the slow negative wave (SNW) and sensory after-discharge (SAD) of the VEP. This effect was detectable at 1 h, reached plateau at 3--4 h and remained at this level 7 h after GVG. Sodium valproate (VPA, di-n-propylacetic acid), which is also believed to block GABA-transaminase and succinic semialdehyde dehydrogenase, when administered in a dose of 200 mg/kg (i.p.) 3 h after GVG reversibly antagonized the SNW-SAD hypersynchronization. The time-course of this effect was similar to that obtained after VPA administration alone. These findings are interpreted as suggesting that VPA acts via a mechanism using a transmitter intimately connected to but not identical with GABA.