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J Neurophysiol 88: 1625-1633, 2002;
0022-3077/02 $5.00
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The Journal of Neurophysiology Vol. 88 No. 4 October 2002, pp. 1625-1633
Copyright ©2002 by the American Physiological Society

Role of Synaptic Metabotropic Glutamate Receptors in Epileptiform Discharges in Hippocampal Slices

Angela C. Lee,1 Robert K. S. Wong,1 Shih-Chieh Chuang,1 Hee-Sup Shin,2 and Riccardo Bianchi1

 1Department of Physiology and Pharmacology, State University of New York, Health Science Center at Brooklyn, Brooklyn, New York 11203; and  2National Creative Research Initiatives Center for Calcium and Learning, Korea Institute of Science and Technology, Seoul, 136-791, Republic of Korea

Lee, Angela C., Robert K. S. Wong, Shih-Chieh Chuang, Hee-Sup Shin, and Riccardo Bianchi. Role of Synaptic Metabotropic Glutamate Receptors in Epileptiform Discharges in Hippocampal Slices. J. Neurophysiol. 88: 1625-1633, 2002. Application of group I metabotropic glutamate receptor (mGluR) agonists elicits seizure discharges in vivo and prolonged ictal-like activity in in vitro brain slices. In this study we examined 1) if group I mGluRs are activated by synaptically released glutamate during epileptiform discharges induced by convulsants in hippocampal slices and, if so, 2) whether the synaptically activated mGluRs contribute to the pattern of the epileptiform discharges. The GABAA receptor antagonist bicuculline (50 µM) was applied to induce short synchronized bursts of ~250 ms in mouse hippocampal slices. Addition of 4-aminopyridine (4-AP; 100 µM) prolonged these bursts to 0.7-2 s. The mGluR1 antagonist (S)-(+)-alpha -amino-4-carboxy-2-methylbenzeneacetic acid (LY 367385; 25-100 µM) and the mGluR5 antagonist 2-methyl-6-(phenylethynyl)pyridine (MPEP; 10-50 µM), applied separately, significantly reduced the duration of the synchronized discharges. The effects of these antagonists were additive when applied together, suggesting that mGluR1 and mGluR5 exert independent actions on the epileptiform bursts. In phospholipase C beta 1 (PLCbeta 1) knockout mice, bicuculline and 4-AP elicited prolonged synchronized discharges of comparable duration as those observed in slices from wild-type littermates. Furthermore, mGluR1 and mGluR5 antagonists reduced the duration of the epileptiform discharges to the same extent as they did in the wild-type preparations. The results suggest that mGluR1 and mGluR5 are activated synaptically during prolonged epileptiform discharges induced by bicuculline and 4-AP. Synaptic activation of these receptors extended the duration of synchronized discharges. In addition, the data indicate that the synaptic effects of the group I mGluRs on the duration of epileptiform discharges were mediated by a PLCbeta 1-independent mechanism.




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