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J Neurophysiol 87: 621-625, 2002;
0022-3077/02 $5.00
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The Journal of Neurophysiology Vol. 87 No. 1 January 2002, pp. 621-625
Copyright ©2002 by the American Physiological Society

RAPID COMMUNICATION

Differential Roles for mGluR1 and mGluR5 in the Persistent Prolongation of Epileptiform Bursts

Lisa R. Merlin

Department of Neurology and Department of Physiology and Pharmacology, The State University of New York Health Science Center at Brooklyn, Brooklyn, New York 11203

Merlin, Lisa R. Differential Roles for mGluR1 and mGluR5 in the Persistent Prolongation of Epileptiform Bursts. J. Neurophysiol. 87: 621-625, 2002. Transient activation of group I metabotropic glutamate receptors (mGluRs) with the selective agonist (S)-3,5-dihydroxyphenylglycine (DHPG) produces persistent prolongation of epileptiform bursts in guinea pig hippocampal slices, the maintenance of which can be reversibly suppressed with group I mGluR antagonists. To determine the relative roles of mGluR1 and mGluR5 in these group I mGluR-dependent induction and maintenance processes, subtype-selective antagonists were utilized. In the presence of picrotoxin, DHPG (50 µM, 20-45 min) converted interictal bursts into 1- to 3-s discharges that persisted for hours following washout of the mGluR agonist. 2-methyl-6-(phenylethynyl)-pyridine (MPEP, an mGluR5 antagonist; 25 µM) and (+)-2-methyl-4-carboxyphenylglycine (LY367385, an mGluR1 antagonist; 20-25 µM) each significantly suppressed the ongoing expression of the mGluR-induced prolonged bursts. However, LY367385 was more effective, reducing the burst prolongation by nearly 90%; MPEP only produced a 64% reduction in burst prolongation. Nevertheless, MPEP was more effective at preventing the induction of the burst prolongation; all 10 slices tested failed to express prolonged bursts both during and after co-application of DHPG with MPEP. Co-application of DHPG with LY367385, in contrast, resulted in significant burst prolongation (in 68% of slices tested) that was revealed on washout of the two agents. These results suggest that while both receptor subtypes participate in both the induction and maintenance of mGluR-mediated burst prolongation, mGluR1 activation plays a greater role in sustaining the expression of prolonged bursts, whereas mGluR5 activation may be a more critical contributor to the induction process underlying this type of epileptogenesis.




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