| Audiogenic seizure susceptibility is induced by termination of continuous infusion of gamma-aminobutyric acid or an N-methyl-D-aspartic acid Antagonist into the inferior colliculus. | |
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MedLine Citation:
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PMID: 11520129 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The inferior colliculus (IC) is strongly implicated in seizure initiation in a genetic form of audiogenic seizures (AGS) and in AGS observed during ethanol withdrawal (ETX). Ethanol is known to block the actions of excitatory amino acids (EAA) and enhance the actions of gamma-aminobutyric acid (GABA) in several brain areas, including the IC. The present study investigated the effects on susceptibility to AGS following withdrawal from continuous blockade of N-methyl-D-aspartic acid (NMDA) receptors or continuous activation of GABA receptors in the IC. This involved infusion of GABA (1 M) or a competitive NMDA antagonist, DL-2-amino-7-phosphonoheptanoic acid (AP7, 1 mM), at 0.25 microl/h for 7 days using an Alzet osmotic minipump. Following abrupt termination of the infusion, AGS susceptibility began at 30 min. The incidence of AGS was 38.9 and 56.3% following GABA and AP7 withdrawal, respectively. The AGS behaviors observed during withdrawal, which included wild running and bouncing clonus, were very similar to those evoked by acoustic stimuli during ETX. AGS susceptibility lasted for several hours and in 13% of animals persisted for up to 6 months. The current results support diminished GABAergic and elevated glutamatergic function in the IC as the critical mechanisms and sites for AGS initiation. The present study, coupled with previous evidence that chronic ethanol exposure reduced GABA-mediated inhibition and enhanced EAA-mediated excitation, suggests that these amino acid receptor-mediated alterations in the IC are key elements in initiating AGS during ethanol withdrawal. |
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Authors:
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L Yang; C Long; C L Faingold |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Experimental neurology Volume: 171 ISSN: 0014-4886 ISO Abbreviation: Exp. Neurol. Publication Date: 2001 Sep |
Date Detail:
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Created Date: 2001-08-24 Completed Date: 2001-10-11 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0370712 Medline TA: Exp Neurol Country: United States |
Other Details:
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Languages: eng Pagination: 147-52 Citation Subset: IM |
Copyright Information:
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Copyright 2001 Academic Press. |
Affiliation:
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Department of Pharmacology, Southern Illinois University School of Medicine, Springfield, Illinois 62794-9629, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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2-Amino-5-phosphonovalerate
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analogs & derivatives Acoustic Stimulation / adverse effects Animals Behavior, Animal / drug effects Catheterization Disease Susceptibility / chemically induced*, complications Drug Administration Routes Epilepsy, Reflex / chemically induced*, complications, physiopathology Excitatory Amino Acid Antagonists* Inferior Colliculi / drug effects*, physiopathology Infusion Pumps, Implantable Male Rats Rats, Sprague-Dawley Reaction Time / drug effects Time Factors gamma-Aminobutyric Acid* |
| Grant Support | |
ID/Acronym/Agency:
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AA11628/AA/NIAAA NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Excitatory Amino Acid Antagonists; 56-12-2/gamma-Aminobutyric Acid; 76726-92-6/2-Amino-5-phosphonovalerate; 85797-13-3/2-amino-7-phosphonoheptanoic acid |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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