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RECORD NUMBER: 28 OF 29

OLS Field Name OLS Field Data
Main Title Systemic Administration of Kainic Acid Increases GABA Levels in Perfusate from the Hippocampus of Rats 'In vivo'.
Author Zhang, W. Q. ; Rogers, B. C. ; Tandon, P. ; Hudson, P. M. ; Sobotka, T. J. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC. Neurotoxicology Div. ;National Inst. of Environmental Health Sciences, Research Triangle Park, NC. Lab. of Molecular and Integrative Neuroscience. ;Food and Drug Administration, Rockville, MD.
Publisher c1990
Year Published 1990
Report Number EPA/600/J-90/522;
Stock Number PB91-211391
Additional Subjects Kainic acid ; Pharmacology ; GABA ; Hippocampus ; In vivo analysis ; Aspartate ; Rats ; Glutamate ; Glutamine ; Glycine ; Taurine ; Nerve cells ; Dose-response relationships ; Reprints ;
Holdings
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NTIS  PB91-211391 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. NTIS 11/26/1991
Collation 10p
Abstract
The ventral hippocampi of male, Fischer-344 rats were implanted with microdialysis probes and the effects of systemically administered kainic acid (KA) (8 mg/kg, s.c.) on the in vivo release of amino acids were measured for four hours after administration. In order to measure GABA release in vivo, gamma-vinyl-GABA (GVG), an irreversible inhibitor of GABA transaminase, was injected intrahippocampally prior to perfusion. GVG pretreatment resulted in measurable levels of GABA in the perfusate without significant effects on the release of aspartate, glutamate, glutamine, glycine or taurine. Following GVG pretreatment systemic administration of KA produced a time-dependent increase in GABA, as well as all other amino acids except glutamine, which was initially decreased. The results show for the first time that systemically administered KA increases extracellular GABA levels, an effect previously reported only in vitro. The data suggest that prior to destruction of GABA-containing interneurons in the hippocampus, there is an increased activity of those GABA interneurons reflected as an increase in extracellular GABA levels. (Copyright (c) 1990 by Intox Press, Inc.)