Source:http://linkedlifedata.com/resource/pubmed/id/12796718
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rdf:type | |
lifeskim:mentions |
umls-concept:C0010286,
umls-concept:C0013879,
umls-concept:C0017462,
umls-concept:C0017639,
umls-concept:C0019564,
umls-concept:C0040300,
umls-concept:C0067684,
umls-concept:C0205332,
umls-concept:C0333641,
umls-concept:C0439810,
umls-concept:C0456603,
umls-concept:C0521390,
umls-concept:C0917805,
umls-concept:C1413038,
umls-concept:C1708237
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pubmed:issue |
6
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pubmed:dateCreated |
2003-6-10
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pubmed:abstractText |
The authors compared temporal profiles of N-acetylaspartate (NAA) and the NAA/total creatine ratio with neuronal and astrocytic densities and with tissue atrophy in the hippocampal CA1 sector of gerbils after 5-minute bilateral forebrain ischemia and subsequent reperfusion for up to 6 months. The CA1 sector was dissected from 20- micro m lyophilized sections (n = 5) for NAA, phosphocreatine, and creatine assays using high-performance liquid chromatography. Adjacent 10- micro m sections were used for immunohistochemical analysis to follow neuronal and astrocytic responses. The NAA concentration was significantly (P<0.01) decreased after 7 days but leveled off thereafter. The NAA/total creatine (phosphocreatine + creatine) ratio was significantly decreased after 7 days and further decreased (P<0.05) after 6 months. Extensive neuronal damage developed beyond 7 days, while reactive astrogliosis progressed throughout the observation period. There was a good linear correlation (P<0.01) between astroglial density and the NAA/total creatine ratio beyond 7 days. The thickness of the CA1 sector was significantly reduced after 1 month and further reduced after 6 months. Although both NAA level and the NAA/total creatine ratio seemed to be indicators of neuronal damage, the latter could be influenced by reactive astrogliosis with progression of tissue atrophy.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0271-678X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
23
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
700-8
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:12796718-Animals,
pubmed-meshheading:12796718-Aspartic Acid,
pubmed-meshheading:12796718-Astrocytes,
pubmed-meshheading:12796718-Atrophy,
pubmed-meshheading:12796718-Cell Count,
pubmed-meshheading:12796718-Common Variable Immunodeficiency,
pubmed-meshheading:12796718-Creatine,
pubmed-meshheading:12796718-Gerbillinae,
pubmed-meshheading:12796718-Gliosis,
pubmed-meshheading:12796718-Hippocampus,
pubmed-meshheading:12796718-Ischemic Attack, Transient,
pubmed-meshheading:12796718-Male,
pubmed-meshheading:12796718-Neurons,
pubmed-meshheading:12796718-Reperfusion Injury
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pubmed:year |
2003
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pubmed:articleTitle |
N-acetylaspartate to total creatine ratio in the hippocampal CA1 sector after transient cerebral ischemia in gerbils: influence of neuronal elements, reactive gliosis, and tissue atrophy.
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pubmed:affiliation |
Department of Neurology, Osaka University Graduate School of Medicine, Osaka, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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