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Impaired glutamate uptake in the R6 Huntington's disease transgenic mice.

Abstract：

:Huntington's disease (HD) is a late-onset neurodegenerative disease for which the mutation is CAG/polyglutamine repeat expansion. The R6 mouse lines expressing the HD mutation develop a movement disorder that is preceded by the formation of neuronal polyglutamine aggregates. The phenotype is likely caused by a widespread neuronal dysfunction, whereas neuronal cell death occurs late and is very selective. We show that a decreased mRNA level of the major astroglial glutamate transporter (GLT1) in the striatum and cortex of these mice is accompanied by a concomitant decrease in glutamate uptake. In contrast, the expression of the glutamate transporters, GLAST and EAAC1, remain unchanged. The mRNA level of the astroglial enzyme glutamine synthetase is also decreased. These changes in expression occur prior to any evidence of neurodegeneration and suggest that a defect in astrocytic glutamate uptake may contribute to the phenotype and neuronal cell death in HD.

journal_name

Neurobiol Dis

journal_title

Neurobiology of disease

authors

Liévens JC,Woodman B,Mahal A,Spasic-Boscovic O,Samuel D,Kerkerian-Le Goff L,Bates GP

doi

10.1006/nbdi.2001.0430

keywords:

subject

Has Abstract

pub_date

2001-10-01 00:00:00

pages

807-21

issue

5

eissn

0969-9961

issn

1095-953X

pii

S0969-9961(01)90430-9

journal_volume

8

pub_type

杂志文章

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