期刊
ASN NEURO
卷 2, 期 2, 页码 -出版社
SAGE PUBLICATIONS LTD
DOI: 10.1042/AN20090058
关键词
excitatory amino acid; Huntington's disease; mouse model; neurodegeneration; striatum; synaptic activity
资金
- United States Public Health Service (USPHS) [NS41574]
- CHDI, Incorporated
- Hereditary Disease Foundation
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS041574] Funding Source: NIH RePORTER
The discovery of the HD (Huntington's disease) gene in 1993 led to the creation of genetic mouse models of the disease and opened the doors for mechanistic studies. In particular, the early changes and progression of the disease could be followed and examined systematically. The present review focuses on the contribution of these genetic mouse models to the understanding of functional changes in neurons as the HD phenotype progresses, and concentrates on two brain areas: the striatum, the site of most conspicuous pathology in HD, and the cortex, a site that is becoming increasingly important in understanding the widespread behavioural abnormalities. Mounting evidence points to synaptic abnormalities in communication between the cortex and striatum and cell-cell interactions as major determinants of HD symptoms, even in the absence of severe neuronal degeneration and death.
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