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It was shown that the preliminary single i.p. injection of antibodies (AB) to glutamate (GLU) 1,5 hours prior to the first injection pentylenetetrazole (prior to the beginning of kindling) did not have an effect on latency period of appearance and the severity of convulsive reactions in the mice of C57Bl/6. The administrations of AB to GLU at the different stages of kindling animals with different severity of seizures did not have an effect on their severity. Thus, AB to GLU did not posses antiepileptic effect. However, AB to GLU posses anticonvulsive action on the acute seizures reaction, inducing an increase in the thresholds of clonic seizures and tonic phase seizures with lethal outcome as well as an extended latency period of occurrance these seizures in mice with enhanced kindling-producing convulsive readiness of the brain. This effect was revealed at the different stages of kindling in animals with the severity of seizures 2-3 and 4-5 marks. Possible to assume, that the mechanisms of chronic epileptogenesis (in this case, in the form kindling-dependent enhanced convulsive readiness of the brain) and those of the acute convulsive reaction are not similar.

In experiments on mice C57Bl/6 was studied the possibility of production of glutamate, GABA, dopamine and serotonin autoantibodies in the dynamics of development of chronic brain epileptization--pharmacological kindling, induced by daily administration of pentylenetetrazol in subconvulsive dose (30 mg/kg) during 24 days. 14 days after the start of the kindling autoantibodies to glutamate was detected in all experimental animals, to CABA--in 60% of mice, to serotonine--in 70%, and to dopamine--in 90%. After 24 days--the number of animals with autoantibodies to glutamate and dopamine was decreased, to serotonin--increased, and to GABA--was not altered. It was shown the relationship between detection neurotransmitters autoantibodies and severity of the convulsive reaction.

The impact of a single intraperitoneal injection of antibodies to glutamate (AG) on acute generalized epileptic activity provoked by systemic introduction of pentilentetrasol was studied in C57B1/6 mice. It was found that AG in doses 10, 25 and 50 mg/kg 1.5 and 24 hours after AG injection produced an anti-epileptic action by raising thresholds of clonic convultions and tonic phase of convultions with lethal outcome and by extending a latent period of their appearance. Later (30 hours after antibodies introduction in a dose 25 mg/kg) AG had no effects on the convulsive reaction thresholds, 48 hours after AG injection they produced a proepileptic effect by lowering the threshold of a clonic convulsion phase.

It was shown that the increased brain seizure readiness persisted within 6 months after termination of corazol kindling. Seizures of the same severity as during kindling (corazol injection in a dose of 20 mg/kg) were reproduced by corazol injection in a dose of 30 mg/kg. In contrast to the control rats, in this situation an autoenhancement of seizures was observed in the kindled animals. Acute corazol seizures induced a decrease in Bmax and Kd of 3H-diazepam binding with benzodiazepine receptors (BDR) in the cerebellum of the 10-months-old control rats white the young animals demonstrated only a decrease in Bmax of binding. In 6 months after kindling termination the BDR activity (Bmax) was reduced by one half. However, we think that the increase in Bmax is not responsible for persistence of the increased seizure readiness. It seems possible that down regulation of receptor activity develops independently of kindling but in response to long-lasting corazol application. Probably, Bmax spontaneously decreases after the termination of the long-term corazol application. The single dose of corazol (30 mg/kg) restores the changes in BDR density to the level when seizure readiness has been just fixed (6 months after kindling termination), independently of the primary receptor density.

The acute korazol (pentylenetetrazol) injection (50 mg/kg) induced seizures which were accompanied by a long-lasting (from 30 minutes to 3 days) decrease in benzodiazepine receptor (BDR) density (Bmax) in rat cerebellum without change in affinity. The density of the BDR was normalized on the 7th day after seizure termination. There were no differences in the initial BDR characteristics between the animals more sensitive to korazol (a dose of 25 mg/kg was sufficient for seizure induction) and less sensitive (30 mg/kg were ineffective). The chronic daily (for 24 days) administration of korazol in a subconvulsive dose led to an increase in seizure readiness (kindling). In 30 min after the last korazol injection the BDR density was decreased to the same extent as after the acute 50 mg/kg korasol administration. The BDR density was normalized on the 7th day after kindling. It was demonstrated that the high-dose-induced and after-kindling seizures were underlain by the same mechanisms. The results suggest that the development of kindling depends on the state of the long-lasting receptors rather than the development of kindling forms the long-lasting reactions. The process of summation is at the basis of kindling development. The long-lasting decrease in activity of BDR receptors induced by a subconvulsive dose of korazol is summed with the following effect of the same dose.