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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
10
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pubmed:dateCreated |
1997-1-17
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pubmed:abstractText |
Previous studies suggest that alterations of brain glutamate synthesis and release occur in experimental thiamine deficiency. In order to assess the integrity of post-synaptic glutamatergic receptors in thiamine deficiency, binding sites for [3H]glutamate (displaced by NMDA), [3H]-kainate, and [3H]quisqualate (AMPA sites) were evaluated using Quantitative Receptor Autoradiography in rat brain following 14 days of treatment with the central thiamine antagonist pyrithiamine. Compared to pair-fed controls, brains of symptomatic thiamine-deficient animals contained significantly fewer NMDA-displaceable binding sites in cerebral cortex, medial septum and hippocampus. It has been suggested that NMDA-receptor mediated glutamate excitotoxicity plays a role in the pathogenesis of neuronal loss in thiamine deficiency. If such is the case, the selective loss of NMDA binding sites in cerebral cortex and hippocampus offers a possible explanation for the relative nonvulnerability of these brain regions to pyrithiamine-induced thiamine deficiency. [3H]quisqualate (AMPA) binding sites were unchanged in all brain regions of pyrithiamine-treated rats whereas [3H]kainate sites were significantly reduced in density in medial and lateral thalamus. The decline in these binding sites may be due to neuronal loss in pyrithiamine-induced thiamine deficiency. Alterations of glutamatergic synaptic function involving both NMDA and kainate receptor subclasses could contribute to the pathogenesis of neurological dysfunction in Wernicke's Encephalopathy in humans.
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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/N-Methylaspartate,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, AMPA,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Glutamate,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Kainic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Tritium
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0364-3190
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
20
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1155-60
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8746800-Animals,
pubmed-meshheading:8746800-Autoradiography,
pubmed-meshheading:8746800-Binding, Competitive,
pubmed-meshheading:8746800-Brain,
pubmed-meshheading:8746800-Male,
pubmed-meshheading:8746800-N-Methylaspartate,
pubmed-meshheading:8746800-Rats,
pubmed-meshheading:8746800-Rats, Sprague-Dawley,
pubmed-meshheading:8746800-Receptors, AMPA,
pubmed-meshheading:8746800-Receptors, Glutamate,
pubmed-meshheading:8746800-Receptors, Kainic Acid,
pubmed-meshheading:8746800-Thiamine Deficiency,
pubmed-meshheading:8746800-Tritium
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pubmed:year |
1995
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pubmed:articleTitle |
Loss of [3H]kainate and of NMDA-displaceable [3H]glutamate binding sites in brain in thiamine deficiency: results of a quantitative autoradiographic study.
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pubmed:affiliation |
Dept of Gerontology, University of Southern California, Los Angeles, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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