Introduction. The investigation of neurotropic drugs — GABA-derivatives effects seems to be interesting especially taking into consideration that GABA participates in CNS functional activity regulation as well as in the cerebral circulation. Additionally it was shown its ability to penetrate through the blood-brain barrier. Both ‘picamilon’ (P) and ‘isopicamilon’ (IP) compounds were synthesized on the background of GABA.

The aim of the work — the investigation of both P and IP influences on mice’s and rat’s behavioural and EEG effects under conditions of picrotoxin-induced generalized convulsive syndrome.

Materials and methods. Trials were performed in conditions of acute and chronic experiment using picrotoxin as traditional convulsive compound that decreases the GABA-induced inhibition. The experimental trials were performed via two series. The 1st devoted to mice’s behavioural convulsive response reactions investigation after P and IP administration in the range 10–100 mg/kg. The 2nd part of the trial was devoted to rats picrotoxin-induced convulsive activity EEG registration after P and IP preliminary administration in the same dosages.

Results. It was shown that IP and P in doses 20–100 mg/kg increase the latency and diminish the intensity of seizures in mice. IP has more expressed anticonvulsant effect that has dose-dependent character.

Both pharmacons preliminary injections in a dose 20 mg/kg resulted in the prevention of generalized ictal discharges generation with subsequent severe clonic-tonic seizures development in rats. IP in a dose 50 mg/kg was more effective in this set of trials revealing the considerable decreasing of frequency and duration of rat’s generalized epileptiform discharges in comparison with P.

Conclusion. The results obtained showed that both P and IP effectively suppressed generalized picrotoxin-induced epileptiform activity in the different strains of the animals. The anticonvulsive effect of the these drugs has dose-dependent character and characterized by seizure latency increasing, seizure intensity decreasing and EEG ictal parameters suppressing comparing with the same indexes of convulsive activity in the control series of the investigation. One could suppose two possible launches in the P and IP mechanisms of anticonvulsive efficacy: the neurotransmitter and metabolic ones that shows the principal mechanism of these drugs control over the seizure activity development and further propagation over the whole brain.

The conclusion was made about P and IP perspectives to be included into the experimental schemes of generalized epileptiform activity complex pathogenetical suppression.