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GABA and Epileptogenesis

y-Aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the CNS. It exerts an inhibitory action in all forebrain structures, and it may play a role in the physiopathogenesis of certain neurological conditions, including epilepsy. Impairment of GABA functions produces seizures, whereas enhancement results in an anticonvulsant effect. Accordingly, several anticonvulsant drugs, including some antiepileptic drugs (AEDs), act by enhancing the efficacy of GABAmediated mechanisms (1,2). Numerous steps in GABA synaptic function are relevant to epileptogenesis: (a) GABA synthesis; (b) GABA release; (c) GABA transport; and (d) activation of receptors, subtypes A and B. Therefore several potential targets exist for epilepsy medications that are related to GABA. GABAA receptors apparently are particularly important in epileptogenesis and therapeutics. Several reviews have described the molecular and functional aspects of GABAA receptors (3-6). In this article, we summarize recent observations, conclusions, and hypotheses regarding the possible role of GABA in epileptogenesis. Much of the information is based on presentations made at the International Symposium “Focus on Epilepsy 111: GABA and Epileptogenesis” held in Whistler, B.C., in May 1995. A list of the faculty that participated in this conference is included in the Notes section.