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Glutamate Dehydrogenase in Cerebellar Mutant Mice: Gene Localization and Enzyme Activity in Different Tissues
Author(s) -
MiretDuvaux Odile,
Frederic Florence,
Simon Dominique,
Guenet JeanLouis,
Hanauer André,
DelhayeBouchaud Nicole,
Mariani Jean
Publication year - 1990
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1990.tb13278.x
Subject(s) - cerebellum , mutant , biology , glutamate dehydrogenase , reeler , purkinje cell , mutation , neuropathology , deep cerebellar nuclei , glutamate receptor , gene , microbiology and biotechnology , genetics , neuroscience , medicine , cerebellar cortex , receptor , disease
Many similarities of both the inheritance pattern and the neuropathology can be observed between olivopontocerebellar atrophies, or so‐called multiple system atrophies (MSAs), and murine cerebellar mutations like Purkinje cell degeneration, nervous, staggerer, weaver, and reeler. Our study aimed to test whether the glutamate dehydrogenase (GDH) deficiency observed in some MSA patients could be found also in any of the murine mutants. GDH activity was assayed in several organs of these mutants, and no general deficiency was detected. By contrast, the level was found to be elevated in the cerebellum. The GDH gene was localized on mouse chromosome 14 and does not map close to any known neurological mutation in the mouse. We conclude, for the moment, that none of these cerebellar mutant mice can be considered as an animal model for GDH‐deficient MSA.