Evidence of a breakdown of corticostriatal connections in Parkinson's disease

被引:197
|
作者
Stephens, B
Mueller, AJ
Shering, AF
Hood, SH
Taggart, P
Arbuthnott, GW
Bell, JE
Kilford, L
Kingsbury, AE
Daniele, SE
Ingham, CA [1 ]
机构
[1] Univ Edinburgh, Div Vet Biomed Sco, Edinburgh EH9 1QH, Midlothian, Scotland
[2] Univ Edinburgh, Royal Dick Sch Vet Studies, Div Neurosci, Edinburgh EH9 1QH, Midlothian, Scotland
[3] Western Gen Hosp, Dept Neuropathol, Edinburgh EH4 2XU, Midlothian, Scotland
[4] UCL, Inst Neurol, Queen Sq Brain Bank, London WC1N 3BG, England
基金
英国惠康基金;
关键词
human brain; caudate putamen; Golgi-impregnation; dendrite; spine; plasticity;
D O I
10.1016/j.neuroscience.2005.01.007
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Dendritic spines are important structures which receive synaptic inputs in many regions of the CNS. The goal of this study was to test the hypothesis that numbers of dendritic spines are significantly reduced on spiny neurones in basal ganglia regions in Parkinson's disease as we had shown them to be in a rat model of the disease [Exp Brain Res 93 (1993) 17]. Postmortem tissue from the caudate and putamen of patients suffering from Parkinson's disease was compared with that from people of a similar age who had no neurological damage. The morphology of Golgi-impregnated projection neurones (medium-sized spiny neurones) was examined quantitatively. The numerical density of dendritic spines on dendrites was reduced by about 27% in both nuclei. The size of the dendritic trees of these neurones was also significantly reduced in the caudate nucleus from the brains of PD cases and their complexity was changed in both the caudate nucleus and the putamen. Dendritic spines receive crucial excitatory input from the cerebral cortex. Reduction in both the density of spines and the total length of the remaining dendrites is likely to have a grave impact on the ability of these neurones to function normally and may partly explain the symptoms of the disorder. (c) 2005 Published by Elsevier Ltd on behalf of IBRO.
引用
收藏
页码:741 / 754
页数:14
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