Microglial responsiveness as a sensitive marker for trimethyltin (TMT) neurotoxicity.

Détails

ID Serval
serval:BIB_B14ABBFC01A6
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Microglial responsiveness as a sensitive marker for trimethyltin (TMT) neurotoxicity.
Périodique
Brain Research
Auteur(s)
Monnet-Tschudi F., Zurich M.G., Pithon E., van Melle G., Honegger P.
ISSN
0006-8993[print], 0006-8993[linking]
Statut éditorial
Publié
Date de publication
08/1995
Volume
690
Numéro
1
Pages
8-14
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
Activation of microglia is a well-documented phenomenon associated with diverse pathological conditions of the central nervous system. In order to investigate the involvement of microglial cells in the neurotoxic action of the heavy metal compound trimethyltin, three-dimensional brain cell cultures were treated during an early developmental period, using concentrations at or below the limit of cytotoxicity. Microglial cells were studied by cytochemical staining, using horseradish peroxidase-conjugated B4 isolectin (GSI-B4). In parallel, neurotoxic effects were assessed by determining the content of synaptophysin and synapsin I, both in the total homogenates and in the synaptosomal fraction of the cultures. Changes in the content of the specific growth cone protein, GAP-43, were also analyzed. It was found that low, non-cytotoxic concentrations of TMT (10(-9) to 10(-8) M) caused a significant increase in the number and/or the clustering of microglial cells. A decrease in the synaptic protein (synapsin I, synaptophysin) content was detected at 10(-8) M of TMT in synaptosomal fractions, whereas in the total homogenates, changes in synaptic proteins and GAP-43 were observed only at the cytotoxic TMT concentration (10(-6) M). Although it remains to be shown whether the microglial response is caused by direct or indirect action of TMT, the present findings show that microglial responsiveness can be detected prior to any sign of neuronal degeneration, and may serve as a sensitive indicator for heavy metal neurotoxicity in the brain.
Mots-clé
Animals, Biological Markers/chemistry, Cell Aging/drug effects, Cell Differentiation/drug effects, Cells, Cultured, GAP-43 Protein, Membrane Glycoproteins/analysis, Microglia/drug effects, Nerve Tissue Proteins/analysis, Rats, Sensitivity and Specificity, Telencephalon/cytology, Telencephalon/drug effects, Trimethyltin Compounds/toxicity
Pubmed
Web of science
Création de la notice
24/01/2008 13:11
Dernière modification de la notice
20/08/2019 15:20
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