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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2002-5-15
pubmed:abstractText
Trimethyltin (TMT) preferentially induces neuronal changes in the hippocampus and pyriform cortex. In the present study we investigated the time course of microglial and astroglial responses associated with neurodegeneration after the administration of TMT (i.p. 9 mg/kg or 12 mg/kg body weight) in the rat. At a dosage of 9 mg/kg TMT, neurodegeneration was clearly demonstrated in the CA1 and CA3 regions of the hippocampus as argyrophilic (dark) neurons by day 4 using the Gallyas-Braak (G-B) impregnation method that has been shown to be sensitive and specific for neurodegeneration. Early microglial response was immunohistochemically shown with anti-microglial response factor-1 (MRF-1) antibody in the CA3 by day 1, preceding neurodegeneration morphologically detected by the G-B method. Activation of astrocytes was revealed by immunohistochemical staining for glial fibrillary acidic protein (GFAP) by day 2. In parallel with the maximal neurodegeneration, large numbers of hypertrophied microglia and astrocytes were observed in the CA1 and CA3 by day 7. Numbers of degenerative neurons appeared to be closely associated with adjacent microglia by the double staining of G-B impregnation and MRF-1 immunohistochemistry. The number of reactive microglia considerably decreased to the resting state by day 14, while hypertrophied astrocytes were still prominent in the CA3 up to day 21. With the high dose of TMT, granule cells in the dentate gyrus and CA1 and CA3 pyramidal cells were significantly impregnated. After TMT treatment, accompaning neurodegeneration we observed early response of microglia and prolonged activation of astrocytes, suggesting an individual role of glial cells in maintenance and repair of damaged neurons following brain injury.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0001-6322
pubmed:author
pubmed:issnType
Print
pubmed:volume
103
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
575-82
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:12012089-Animals, pubmed-meshheading:12012089-Astrocytes, pubmed-meshheading:12012089-Body Weight, pubmed-meshheading:12012089-Calcium-Binding Proteins, pubmed-meshheading:12012089-Glial Fibrillary Acidic Protein, pubmed-meshheading:12012089-Gliosis, pubmed-meshheading:12012089-Hippocampus, pubmed-meshheading:12012089-Immunohistochemistry, pubmed-meshheading:12012089-Male, pubmed-meshheading:12012089-Microfilament Proteins, pubmed-meshheading:12012089-Microglia, pubmed-meshheading:12012089-Nerve Degeneration, pubmed-meshheading:12012089-Nerve Regeneration, pubmed-meshheading:12012089-Nerve Tissue Proteins, pubmed-meshheading:12012089-Neurons, pubmed-meshheading:12012089-Rats, pubmed-meshheading:12012089-Rats, Sprague-Dawley, pubmed-meshheading:12012089-Trimethyltin Compounds
pubmed:year
2002
pubmed:articleTitle
Neuronal degeneration and glial cell-responses following trimethyltin intoxication in the rat.
pubmed:affiliation
Department of Schizophrenia Research, Division of Psychiatric Disorders Research, Tokyo Institute of Psychiatry, 2-1-8 Kamikitazawa, Setagaya-ku 156-8585, Japan. shaga@prit.go.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't