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.
D000612:4-Aminobutyrate Transaminase / Q000037:antagonists & inhibitors*; D000614:Aminocaproates / Q000494:pharmacology*; D000818:Animals; D005074:Evoked Potentials, Visual / Q000187:drug effects*; D005260:Female; D008297:Male; D009457:Neuroglia / Q000032:analysis; D051381:Rats; D011919:Rats, Inbred Strains; D000637:Transaminases / Q000037:antagonists & inhibitors*; D014635:Valproic Acid / Q000494:pharmacology*; D020888:Vigabatrin; D005680:gamma-Aminobutyric Acid / Q000032:analysis / Q000502:physiology
D000614:Aminocaproates; D005680:gamma-Aminobutyric Acid; D014635:Valproic Acid; D000637:Transaminases; D000612:4-Aminobutyrate Transaminase; D020888:Vigabatrin