Pharmacologic analysis of sodium valproate-induced suppression of secondary components of visual evoked potentials in albino rats.
Sodium Valproate (VPA) administered to rats in a dose of 10 or 200 mg/kg IP suppressed the slow negative wave (SNW) and photically-induced afterdischarge (SAD) of VEP (when they were present) within 15-30 min. The recovery of VEP amplitude began at 3 hr. This effect was antagonized by subconvulsive doses of convulsant benzodiazepine RO 5-3663 (2 mg/kg) and metrazol (15 mg/kg) but not by picrotoxin (2 mg/kg) and naloxone (10 mg/kg). The SNW suppression may be attributed to a disinhibitory action of a system located presynaptically on recurrent collaterals of the output neurons, or nerve terminals of inhibitory interneurons or both. Alternative conjecture suggests that VPA depolarizes the dendritic tree masking thereby somatic inhibition produced by recurrent circuits.
D000818:Animals; D001570:Benzodiazepinones / Q000494:pharmacology; D003292:Convulsants / Q000494:pharmacology; D004347:Drug Interactions; D005074:Evoked Potentials, Visual / Q000187:drug effects*; D005260:Female; D008297:Male; D009270:Naloxone / Q000494:pharmacology; D010433:Pentylenetetrazole / Q000494:pharmacology; D010775:Photic Stimulation; D010852:Picrotoxin / Q000494:pharmacology; D051381:Rats; D009435:Synaptic Transmission / Q000187:drug effects; D013997:Time Factors; D014635:Valproic Acid / Q000494:pharmacology*; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D001570:Benzodiazepinones; D003292:Convulsants; D009270:Naloxone; D010433:Pentylenetetrazole; D010852:Picrotoxin; D014635:Valproic Acid; D005680:gamma-Aminobutyric Acid; C022193:Ro 5-3663