Limbic neurogenesis/plasticity in the R6/2 mouse model of Huntington's disease

被引:16
作者
Phillips, Wendy
Morton, A. Jennifer
Barker, Roger A.
机构
[1] Cambridge Ctr Brain Repair, Cambridge CB2 2PY, England
[2] Addenbrookes Hosp, Dept Neurol, Cambridge, England
[3] Univ Cambridge, Dept Pharmacol, Cambridge CB2 1QJ, England
基金
英国医学研究理事会;
关键词
doublecortin; Huntington's disease; insula; limbic system; neurogenesis; piriform cortex; R6/2; seizures;
D O I
10.1097/01.wnr.0000236855.85962.f6
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Huntington's disease is an inherited neurodegenerative condition characterized by movement disorders, and mood and cognitive disturbance. Mammalian neurogenesis persists into adulthood in the subventricular zone and dentate gyrus of the hippocampus. Neurogenesis is abnormal in the dentate gyrus in the R6/2 transgenic mouse model of Huntington's disease. We have now found that the number of immature neurons (doublecortin-positive cells) is markedly reduced in the piriform and insular cortex but not in the temporal germinal layer or caudal subventricular zone of R6/2 mice. Furthermore, numbers of such cells were unaltered in response to seizures in both wild-type and R6/2 mice. These results support the possibility that impaired neurogenesis and/or plasticity could contribute to cognitive and psychiatric impairments in Huntington's disease.
引用
收藏
页码:1623 / 1627
页数:5
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