Abstract
Intraperitoneal administration of pirlindole (pirazidole) or ‘soluble pirlindole’ 50 mg/kg body-weight prolonged the onset of seizures and decreased the intensity of seizures in rats genetically selected for high sensitivity to audiogenic hereditary epilepsy [Krushinsky-Molodkina (KM) rats]. In this experimental model of epilepsy, pirlindole prevented qualitative alteration (transformation) in the catalytic activity of membrane-bound type A monoamine oxidases (MAO-A), pathogenetically important for the development of the audiogenic seizures. Modification of the enzymatic properties of the monoamine oxidases causes an increase in γ-aminobutyric acid (GABA) deamination in the mitochondrial fraction of the brain. The data obtained suggest that selective inhibitors of MAO-A, such as pirlindole, may prevent experimental epileptic seizures.
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