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The Journal of Neurophysiology Vol. 82 No. 2 August 1999, pp. 1078-1081
Copyright ©1999 by the American Physiological Society
RAPID COMMUNICATION
Department of Neurology and Department of Physiology and Pharmacology, State University of New York Health Science Center at Brooklyn, Brooklyn, New York 11203
Merlin, Lisa R.
Group I mGluR-Mediated Silent Induction of Long-Lasting
Epileptiform Discharges. J. Neurophysiol. 82: 1078-1081, 1999. Picrotoxin, an antagonist of GABAA
receptor-mediated activity, elicited 320- to 475-ms synchronized bursts
from the CA3 region of the guinea pig hippocampal slice. The addition
of the selective group I metabotropic glutamate receptor (mGluR)
agonist (S)-3,5-dihydroxyphenylglycine (DHPG, 50 µM;
20- to 45-min application) gradually increased the burst duration to
1-4 s; this effect persisted 2-3 h after agonist removal. To
determine whether the induction of this long-lasting effect required
ongoing synchronized activity during mGluR activation, DHPG application
in a second set of experiments took place in the presence of CNQX and
(R,S)-CPP, antagonists of AMPA/kainate and NMDA
receptors, respectively. In these experiments, synchronized bursting
was silenced during the mGluR agonist application, yet after wash out
of the DHPG and the ionotropic glutamate receptor (iGluR) blockers,
epileptiform discharges 1-10 s in duration appeared and persisted at
least 2 h after wash out of the mGluR agonist. The potentiated
bursts were reversibly shortened by application of 500-1,000 µM
(+)-
-methyl-4-carboxyphenylglycine (MCPG) or (S)-4-carboxyphenylglycine (4CPG), agents with group I
mGluR antagonist activity. These data suggest that transient activation
of group I mGluRs, even during silencing of synchronized epileptiform
activity, may have an epileptogenic effect, converting brief
interictal-length discharges into persistent seizure-length events. The
induction process is iGluR independent, and the maintenance is largely
mediated by the action of endogenous glutamate on group I mGluRs,
suggesting that autopotentiation of the group I mGluR-mediated response
may underlie the epileptogenesis seen here.
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