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Elevated γ‐Aminobutyric Acid Levels Attenuate the Metabolic Response to Biateral Ischemia
Author(s) -
Abel Marc S.,
McCandless David W.
Publication year - 1992
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1992.tb09780.x
Subject(s) - ischemia , vigabatrin , aminobutyric acid , medicine , endocrinology , glycogen , chemistry , pharmacology , anesthesia , biology , anticonvulsant , epilepsy , neuroscience , receptor
Bilateral ischemia has been shown to alter the net brain levels of energy metabolites such as ATP, phosphocre‐atine, glucose, and glycogen. The amino acid neurotrans‐mitter γ‐aminobutyric acid (GABA) exerts a tonic inhibitory influence on neural activity. The present studies were designed to evaluate the influence of elevated GABA levels on the metabolic sequelae of ischemia. The GABA transaminase inhibitor γ‐vinyl‐GABA (GVG; vigabatrin) was administered to Mongolian gerbils before the production of a bilateral ischemic incident. GABA levels were elevated in all regions assayed. Levels of energy metabolites were also increased, an indication of reduced energy utilization. In control animals, in the absence of GVG, 1 min of bilateral ischemia produced decreases in the levels of all metabolites. In animals pretreated with GVG, the effects of 1 min of bilateral ischemia were attenuated. These data suggest that the level of ongoing activity may affect the response to an ischemic insult. Furthermore, GVG may have a clinical indication in reducing the effect of minor ischemic incidents.