Source:http://linkedlifedata.com/resource/pubmed/id/12468891
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
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pubmed:dateCreated |
2002-12-6
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pubmed:abstractText |
Impairment of inhibitory neurotransmission has been reported to occur in widespread, structurally intact brain regions after focal ischemic stroke. These long-lasting alterations contribute to the functional deficit and influence long-term recovery. Inhibitory neurotransmission is primarily mediated by gamma-aminobutyric acid (GABA)A receptors assembled of five subunits that allow a variety of adaptive changes. In this study, the regional distribution of five major GABA(A)-receptor subunits (alpha1, alpha2, alpha3, alpha5, and gamma2) was analyzed immunohistochemically 1, 7, and 30 days after photochemically induced cortical infarcts. When compared with sham-operated controls, a general and regionally differential reduction in immunostaining was found within the cortex, hippocampus, and thalamus of both hemispheres for almost all subunits. Within ipsilateral and contralateral neocortical areas, a specific pattern of changes with a differential decrease of subunits alpha1, alpha2, alpha5, and gamma2 and a significant upregulation of subunit alpha3 was observed in the contralateral cortex homotopic to the infarct. This dysregulation was most prominent at day 7 and still present at day 30. Interestingly, a single application of the noncompetitive N-methyl-D-aspartate-receptor antagonist MK-801 during lesion induction completely blocked these bihemispheric alterations. Cortical spreading depressions induced by topical application of KCl do not change GABA(A)-receptor subunit expression. As alterations in subtype distribution crucially influence inhibitory function, ischemia-induced modifications in GABA(A)-receptor subtype expression may be of relevance for functional recovery after stroke.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Dizocilpine Maleate,
http://linkedlifedata.com/resource/pubmed/chemical/Excitatory Amino Acid Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, GABA-A,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, N-Methyl-D-Aspartate
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0271-678X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
22
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1463-75
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:12468891-Animals,
pubmed-meshheading:12468891-Cerebral Infarction,
pubmed-meshheading:12468891-Cortical Spreading Depression,
pubmed-meshheading:12468891-Dizocilpine Maleate,
pubmed-meshheading:12468891-Excitatory Amino Acid Antagonists,
pubmed-meshheading:12468891-Functional Laterality,
pubmed-meshheading:12468891-Hippocampus,
pubmed-meshheading:12468891-Intracranial Thrombosis,
pubmed-meshheading:12468891-Male,
pubmed-meshheading:12468891-Neocortex,
pubmed-meshheading:12468891-Rats,
pubmed-meshheading:12468891-Rats, Wistar,
pubmed-meshheading:12468891-Receptors, GABA-A,
pubmed-meshheading:12468891-Receptors, N-Methyl-D-Aspartate,
pubmed-meshheading:12468891-Thalamus
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pubmed:year |
2002
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pubmed:articleTitle |
Widespread and long-lasting alterations in GABA(A)-receptor subtypes after focal cortical infarcts in rats: mediation by NMDA-dependent processes.
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pubmed:affiliation |
Department of Neurology, Friedrich-Schiller-University, Philosophenweg 3, D-07743 Jena, Germany. redecker@ med.uni-jena.de
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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