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Previous Article | Next Article
Volume 16, Number 12, Issue of June 15, 1996 pp. 3912-3924
Copyright ©1996 Society for NeuroscienceSynchronous GABA-Mediated Potentials and Epileptiform Discharges in the Rat Limbic System In Vitro
Received Dec. 20, 1995; revised March 14, 1996; accepted March 29, 1996.
Massimo Avoli1, Michaela Barbarosie1, Anne Lücke2, Takeki Nagao3, Valeri Lopantsev1, and Rüdiger Köhling2 1 Montreal Neurological Institute and Departments of Neurology, Neurosurgery, and Physiology, McGill University, Montreal, Quebec, Canada H3A 2B4, 2 Institut für Physiologie, Universität, 48149 Münster, Germany, and 3 Department of Neurosurgery, Tokyo Women's Medical College, Shinjuku-ku, Tokyo, 162, Japan
Application of 4-aminopyridine (4AP, 50 µM) to combined slices of adult rat hippocampus-entorhinal cortex-induced ictal and interictal epileptiform discharges, as well as slow field potentials that were abolished by the µ-opioid agonist [D-Ala2,N-Me-Phe4,Gly-ol5] enkephalin (DAGO, 10 µM) or the GABAA receptor antagonist bicuculline methiodide (BMI, 10 µM); hence, they represented synchronous GABA-mediated potentials. Ictal discharges originated in the entorhinal cortex and propagated to the hippocampus, whereas interictal activity of CA3 origin was usually recorded in the hippocampus. The GABA-mediated potentials had no fixed site of origin or modality of propagation; they closely preceded (0.2-5 sec) and thus appeared to initiate ictal discharges. Only ictal discharges were blocked by the antagonist of the NMDA receptor 3,3-(2-carboxypiperazine-4-yl)propyl-1-phosphonate (CPP, 10 µM), whereas the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 µM) abolished all epileptiform activities. The GABA-mediated potentials continued to occur synchronously in all regions even after concomitant application of CNQX and CPP. [K+]o elevations were recorded in the entorhinal cortex during the ictal discharge (peak values = 13.9 ± 0.9 mM) and the synchronous GABA-mediated potentials (peak values = 4.2 ± 0.1 mM); the latter increases were presumably attributable to postsynaptic GABAA-receptor activation because they were abolished by DAGO or BMI. Their role in initiating ictal activity was demonstrated by using DAGO, which abolished both GABA-mediated synchronous potentials and ictal discharges. These data indicate that NMDA-mediated ictal discharges induced by 4AP originate in the entorhinal cortex; such a conclusion is in line with clinical evidence obtained in temporal lobe epilepsy patients. 4AP also induces GABA-mediated potentials that spread within the limbic system when excitatory transmission is blocked and may play a role in initiating ictal discharge by increasing [K+]o.
Key words: entorhinal cortex; seizures; GABA; excitatory amino acids; rat; 4-aminopyridine
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