Glutamate Receptors in Epilepsy

Riccardo Bianchi, Robert K. S. Wong and Lisa R. Merlin

in Jasper's Basic Mechanisms of the Epilepsies

Fourth edition

Published on behalf of ©Jeffrey L. Noebels, Massimo Avoli, Michael A. Rogawski, Richard W. Olsen, and Antonio V. Delgado-Escueta

Published in print July 2012 | ISBN: 9780199746545
Published online April 2013 | e-ISBN: 9780199322817 | DOI:

Series: Contemporary Neurology Series

Glutamate Receptors in Epilepsy

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In the early 1990s, the epileptogenic potential of metabotropic glutamate receptor (mGluR) activation in the hippocampus was first suggested by data using the then newly developed broad- spectrum mGluR agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD).1 These studies revealed that mGluR activation had the potent ability to recruit the hippocampal network to express robust synchronized discharges. These synchronized bursts had features suggestive of typical seizure discharges in that (1) their length was on the order of seconds and (2) they were comprised of an intrinsic oscillatory series of discharges that began at a high frequency and gradually slowed. And indeed, work in other labs confirmed that ACPD application does elicit seizures in the intact organism.2 A hypothesis was developed proposing that the group I mGluRs, which are predominantly localized to the edges of synapses (perisynaptic),3 were likely to be activated at times of intense glutamate release, and this could result in the expression of acute seizures such as the impact seizure that occurs acutely in the setting of head trauma. However, subsequent studies using the selective group I mGluR agonist (S)-3,5-dihydroxyphenylglycine (DHPG) revealed a potential additional consequence of group I mGluR activation: long- lasting changes in network excitability.4

Chapter.  6232 words.  Illustrated.

Subjects: Neurology

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