Journal
NEUROBIOLOGY OF DISEASE
Volume 41, Issue 2, Pages 570-576Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2010.09.021
Keywords
Adenosine receptor; A(2A); Huntington's disease; N171-82Q; Transgenic model; Striatum
Categories
Funding
- Interuniversity Attraction Poles Programme (P6-14), Belgian State, Belgian Science Policy
- Fondation Medicale Reine Elisabeth
- Walloon Region (Programme d'Excellence CIBLES)
- Fonds National de la Recherche Scientifique
- INSERM
- CNRS
- IMPRT
- University of Lille 2
- Lille County Hospital (CHRU-Lille)
- Region Nord-Pas-de-Calais
- ANR [ANR JC07_184902/ADONTAGE]
- Hereditary Disease Foundation
- FRIA
- Fondation Van Buuren
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Huntington's disease (HD) is a progressive neurodegenerative genetic disorder that leads to motor, cognitive, and psychiatric disturbances. The primary neuropathological hallmark is atrophy of the striatum. HD preferentially affects efferent striato-pallidal neurons that express enkephalin as well as dopamine D2 and A(2A) adenosine receptors (A(2A)Rs). Expression and function of A(2A)Rs are altered in HD but, despite being an important modulator of the striato-pallidal function, the subsequent pathophysiological consequence of such changes remains unclear. Whether blockade of A(2A)Rs is of therapeutic interest in HD remains ill-defined. In the present work, we aimed to determine the pathophysiological consequences of genetic deletion of A(2A)Rs in HD by crossing A(2A)R knockout mice with the N171-82Q HD transgenic model. Our data demonstrate that knockout of A(2A)Rs moderately but significantly worsens motor performances and survival of N171-82Q mice and leads to a decrease in striatal enkephalin expression. These results support that early and chronic blockade of A(2A)Rs might not be beneficial in HD. (c) 2010 Elsevier Inc. All tights reserved.
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