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• W2108461170 endingPage "2914" @default.
• W2108461170 startingPage "2901" @default.
• W2108461170 abstract "ABSTRACT We tested the hypothesis that the neurotransmitter glutamate would influence glial proliferation and differentiation in a cytoarchitecturally intact system. Postnatal day 6 cerebellar slices were maintained in organotypic culture and treated with glutamate receptor agonists or antagonists. After dissociation, cells were stained with antibodies for different oligodendrocyte developmentally regulated antigens. Treatment of the slices with the glutamate receptor agonists kainate or α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid significantly decreased the percentage of LB1+, NG2+ and O4+ cells, and their bromodeoxyuridine labeling index. The non-N-methyl-D-aspartate glutamate receptor antagonist 6,7-dinitroquinoxaline-2,3-dione increased the percentage and bromodeoxyuridine labeling of LB1+, NG2+ and O4+ cells. In intact slices, RNA levels of the oligodendrocyte gene for 2’,3’-cyclic nucleotide 3’-phosphodiesterase were decreased by kainate and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, and increased by 6,7-dinitroquinoxaline-2,3-dione. The percentage of astrocytes was not modified by kainate, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid or 6,7-dinitroquinoxaline-2,3-dione. Treatment with the N-methyl-D-aspartate receptor antagonist 2-amino-5-phosphonopentanoic acid did not alter the percentage of O4+ cells, nor their proliferation. Incubation with the γ-aminobutyric acid receptor antagonist bicuculline did not modify the percentage of LB1+, A2B5+ and O4+ cells. In purified cerebellar oligodendrocyte progenitor cells, glutamate receptor agonists blocked K+ currents, and inhibited cell proliferation and lineage progression. The K+ channel blocker tetraethylammonium also inhibited oligodendrocyte progenitor cell proliferation. These findings indicate that in rat cerebellar tissue slices: (i) glutamate specifically modulates oligodendrocyte but not astrocyte development through selective activation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, and (ii) cell depolarization and blockage of voltage-dependent K+ channels is likely to be the triggering mechanism." @default.
• W2108461170 created "2016-06-24" @default.
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• W2108461170 date "1998-08-01" @default.
• W2108461170 modified "2023-10-12" @default.
• W2108461170 title "A role for glutamate and its receptors in the regulation of oligodendrocyte development in cerebellar tissue slices" @default.
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• W2108461170 doi "https://doi.org/10.1242/dev.125.15.2901" @default.
• W2108461170 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9655812" @default.
• W2108461170 hasPublicationYear "1998" @default.
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