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Distinctions between persistent and reversible group I mGluR‐induced epileptiform burst prolongation
Author(s) -
Fuortes Michaelangelo G.,
Rico Marjorie J.,
Merlin Lisa R.
Publication year - 2010
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1167.2010.02682.x
Subject(s) - metabotropic glutamate receptor , agonist , neuroscience , metabotropic receptor , quisqualic acid , acpd , chemistry , nmda receptor , glutamate receptor , biology , receptor , ampa receptor , biochemistry
Summary We have previously shown that selective activation of group I metabotropic glutamate receptors (mGluRs) results in long‐lasting enhancement of synchronized network activity in the hippocampal slice. Data herein suggest that activation of group I mGluRs need not result in this potentially epileptogenic effect. (1S,3R)‐1‐Aminocyclopentane‐1,3‐dicarboxylic acid (ACPD), a nonselective mGluR agonist, elicits ictaform bursts identical in appearance to those induced by selective agonists, but ACPD‐induced bursts do not persist following removal of the agent. Like the bursts induced by selective agonist, the ACPD bursts are blocked with group I mGluR antagonists and are not dependent on activation of either N‐methyl‐ d ‐aspartate (NMDA) receptors or protein kinase C. However, they differ from the persistent bursts in that they do not require active protein synthesis and they are not suppressed with L‐cysteine sulfinic acid, an agonist at a phospholipase D‐coupled metabotropic receptor. These novel findings provide evidence that group I mGluR‐induced epileptogenesis may be preventable.