Release of exogenous γ-[³H]aminobutyric acid during seizure activity in chronically denervated and normal cat cortex

Abstract

The hypothesis that the seizure susceptibility of chronically denervated cortex is due to interruption of recurrent inhibitory pathways was tested by examining the release of 3H-labeled γ-aminobutyric acid ([3H]GABA) from chronic slabs and normal cortex of cats. Seizure activity was maintained throughout the test periods in both normal and chronically isolated cortex. When methacholine was used to evoke seizure activity, [3H]GABA release was depressed in both normal and epileptic cortex, suggesting that the mechanism of seizure genesis by cholinomimetics involves suppression of inhibitory neuron activity. Pentylenetetrazol-induced seizures evoked a small, equal increase in [3H]GABA efflux from epileptic and normal cortex. Continuous electrical stimulation evoked a large, and again equal increase in [3H]GABA release. Preseizure efflux of [3H]GABA was the same from chronic slabs and normal cortex in all experiments. Since the interruption of recurrent inhibitory pathways by chronic denervation would result in a decreased resting and seizure-evoked release of [3H]GABA, results obtained do not support the above-mentioned hypothesis. </jats:p