Document Detail


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.
MedLine Citation:
PMID:  7522389     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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 glutamic acid decarboxylase, and cytochrome c oxidase and ATP synthase, while the astrocytes showed an enhanced immunoreactivity for GFAP. The diverse patterns of enhanced immunoreactivity suggested, furthermore, a wider low-to-high range of metabolic activities in both excitatory and inhibitory neurons.
Authors:
H J Romijn; A W Janszen; C Van den Bogert
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Acta neuropathologica     Volume:  87     ISSN:  0001-6322     ISO Abbreviation:  Acta Neuropathol.     Publication Date:  1994  
Date Detail:
Created Date:  1994-10-17     Completed Date:  1994-10-17     Revised Date:  2007-11-09    
Medline Journal Info:
Nlm Unique ID:  0412041     Medline TA:  Acta Neuropathol     Country:  GERMANY    
Other Details:
Languages:  eng     Pagination:  612-27     Citation Subset:  IM    
Affiliation:
Graduate School Neurosciences Amsterdam, Netherlands Institute for Brain Research.
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn / physiology*
Anoxia / metabolism*
Brain Ischemia / metabolism*
Cerebral Cortex / metabolism*
Electron Transport Complex IV / metabolism*
Glial Fibrillary Acidic Protein / metabolism
Glutamate Decarboxylase / metabolism*
Immunohistochemistry / methods
Isoenzymes / metabolism
Mitochondria / enzymology
Proton-Translocating ATPases / metabolism
Rats
Rats, Wistar
Staining and Labeling
gamma-Aminobutyric Acid / metabolism*
Chemical
Reg. No./Substance:
0/Glial Fibrillary Acidic Protein; 0/Isoenzymes; 56-12-2/gamma-Aminobutyric Acid; EC 1.9.3.1/Electron Transport Complex IV; EC 3.6.3.14/Proton-Translocating ATPases; EC 4.1.1.15/Glutamate Decarboxylase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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