GABA sub(A)/benzodiazepine receptor gamma sub(2) subunit gene expression in developing normal and mutant mouse cerebellum
Recent studies have identified several subunits ( alpha , beta , gamma and delta ) of the gamma -aminobutyric acid sub(A)/benzodiazepine receptor; each consists of several variants. The gamma sub(2) subunit appears to mediate the interaction of the alpha and beta subunits making the receptor capable...
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Published in | Brain research. Molecular brain research. Vol. 19; no. 1-2; pp. 9 - 21 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
01.01.1993
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Online Access | Get full text |
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Summary: | Recent studies have identified several subunits ( alpha , beta , gamma and delta ) of the gamma -aminobutyric acid sub(A)/benzodiazepine receptor; each consists of several variants. The gamma sub(2) subunit appears to mediate the interaction of the alpha and beta subunits making the receptor capable of modulation by benzodiazepines. In the present studies, the expression of mRNA encoding the gamma sub(2) subunit was examined in the cerebellum during development and in adult Purkinje cell degeneration, lurcher and reeler mutant mice. In the normal adult cerebellum, in situ hybridization with [ super(35)S]cRNA probes revealed a strong signal over the Purkinje cell layer and deep cerebellar nuclei, and a weaker signal over basket, stellate and granule cells. In adult Purkinje cell degeneration and lurcher mutants, in which Purkinje cells have degenerated, no punctate labeling characteristic of mature Purkinje cells was detected. In adult and developing reeler mutants, where all classes of cells are malpositioned throughout the cerebellum, the punctate hybridization signal was present and clearly associated with Purkinje cells in all cortical regions. Our results suggest that developing Purkinje cells express the gamma sub(2) gene at a time prior to receiving GABAergic inhibitory input, and that the continued expression in the adult is not affected by the absence of afferents. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 content type line 23 ObjectType-Feature-1 |
ISSN: | 0169-328X |