PMID: 7522389Jan 1, 1994Paper

Permanent increase of immunocytochemical reactivity for gamma-aminobutyric acid (GABA), glutamic acid decarboxylase, mitochondrial enzymes, and glial fibrillary acidic protein in rat cerebral cortex damaged by early postnatal hypoxia-ischemia

Acta Neuropathologica
H J RomijnC Van den Bogert

Abstract

A former study indicated that hypoxic-ischemic encephalopathy in rat sustained during early postnatal life may result in permanent epileptic activity in the baseline electroencephalogram. We, therefore, investigated whether the presumed higher firing frequency and metabolic activity of neurons in such hypoxia-damaged cortical areas would be reflected by an enhanced light microscopic immunoreactivity of gamma-aminobutyric acid (GABA), the two isoforms of glutamic acid decarboxylase (GAD67 and GAD65), the mitochondrial enzymes cytochrome c oxidase and ATP synthase, and/or glial fibrillary acidic, protein (GFAP). To that end rat pups, 12-13 days of age, were unilaterally exposed to hypoxic-ischemic conditions and, after a survival period of 2 and 6 1/2 months, respectively, killed by perfusion fixation. After dissection of the brain, coronal vibratome sections of animals showing cortical damage were immunostained for the presence of the above-mentioned antigens. Subsequent qualitative analysis revealed that the surroundings of cortical infarctions were unambiguously characterized by a disordered neural network containing numerous nerve cells, fibers and/or endings showing an enhanced immunoreactivity for GABA, both isoforms of glu...Continue Reading

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Citations

Oct 6, 1997·Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism·A Fergus, K S Lee
Oct 1, 1996·Stroke; a Journal of Cerebral Circulation·Z KovácsM Fukui
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Feb 25, 1998·Pediatric Research·E C MallardR Harding
Nov 25, 1997·Annals of the New York Academy of Sciences·Z Binienda

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