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 BYEARLY POSTNATAL HYPOXIA-ISCHEMIA

A former study indicated that hypoxic-ischemic encephalopathy in rat s ustained during early postnatal life may result in permanent epileptic activity in the baseline electroencephalogram. We, therefore, investi gated whether the presumed higher firing frequency and metabolic activ ity of neurons in such hypoxia-damaged cortical areas would be reflect ed by an enhanced light microscopic immunoreactivity of gamma-aminobut yric acid (GABA), the two isoforms of glutamic acid decarboxylase (GAD (67) and GAD(65)), 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 61/2 months, respectively, killed by perfusion fixation. After dissection of the b rain, coronal vibratome sections of animals showing cortical damage we re immunostained for the presence of the above-mentioned antigens. Sub sequent qualitative analysis revealed that the surroundings of cortica l 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 glutamic acid decarboxylase, and cytochrome c oxidase and ATP synthase, while the a strocytes showed an enhanced immunoreactivity for GFAP. The diverse pa tterns of enhanced immunoreactivity suggested, furthermore, a wider lo w-to-high range of metabolic activities in both excitatory and inhibit ory neurons.