We studied the effect of single intraperitoneal treatment with antibodies to glutamate on pentylenetetrazole-induced acute generalized epileptiform activity in C57Bl/6 mice. The antiepileptic effect was observed 1.5 and 24 h after administration of antibodies to glutamate in doses of 10, 25, and 50 mg/kg. This treatment increased the thresholds of clonic seizures and tonic phase of seizures with lethal outcome.
Experiments on Wistar rats showed that muscimol-stimulated Cl(-) conduction of synaptoneurosomes, isolated from the cerebral cortex increased after 5-day systemic treatment with subconvulsive doses of pentylene tetrasole during the initial stage of pharmacological pentylene tetrasole kindling, characterized by gradually augmenting convulsive readiness of the brain. This indicates an increase in functional activity of the GABA(A) receptor/Cl(-) ionophore complex.
Experiments on C57Bl/6 mice showed that chronic epileptization of the brain (pharmacological pentylenetetrazole kindling) is accompanied by induction of autoantibodies against glutamate and GABA. Immunohistochemical similarity of antibodies against glutamate and GABA was demonstrated. Study on the model of pentylenetetrazole-induced acute generalized epileptiform activity showed high immunobiological specificity of intraperitoneally injected antibodies against GABA and glutamate: antiepileptic effect of antiglutamate antibodies and proepileptic effect of antibodies against GABA.
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