Impaired learning-dependent cortical plasticity in Huntington's disease transgenic mice

被引:31
作者
Cybulska-Klosowicz, A
Mazarakis, NK
Van Dellen, A
Blakemore, C
Anthony, AJ
Kossut, M
机构
[1] M Nencki Inst Expt Biol, Lab Neuroplastic, PL-02093 Warsaw, Poland
[2] Univ Oxford, Physiol Lab, Oxford OX1 3PT, England
[3] Univ Melbourne, Howard Florey Inst Expt Physiol & Med, Parkville, Vic 3010, Australia
关键词
Huntington's disease; barrel cortex; associative learning; plasticity; 2-deoxyglucose autoradiography;
D O I
10.1016/j.nbd.2004.08.009
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Huntington's disease (HD) is a genetically transmitted neurodegenerative disorder. The neuropathology in HD is a selective neuronal cell death in several brain regions including cortex. Although changes in synaptic plasticity were shown within the hippocampus and striatum of HD transgenic mice, there are no studies considering neocortical synaptic plasticity abnormalities in HD. We examined the impact of the HD transgene upon learning-dependent plasticity of cortical representational maps. The effect of associative learning, in which stimulation of a row of vibrissae was paired with appetitive stimulus, upon functional representations of vibrissae in the barrel cortex, was investigated with 2-deoxyglucose brain mapping in presymptomatic R6/1 HD mice. In wild-type mice, cortical representation of the row of vibrissae involved in the training was expanded, while in HD mice the representation of this row was not expanded. The results suggest that presymptomatic R6/1 HD transgenic mice show deficits in plasticity of primary somatosensory cortex. (C) 2004 Elsevier Inc. All rights reserved.
引用
收藏
页码:427 / 434
页数:8
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