Deficits induced by quinolinic acid lesion to the striatum in a position discrimination and reversal task are ameliorated by permanent and temporary lesion to the globus pallidus: A potential novel treatment in a rat model of Huntington's disease
Deficits induced by quinolinic acid lesion to the striatum in a position discrimination and reversal task are ameliorated by permanent and temporary lesion to the globus pallidus: A potential novel treatment in a rat model of Huntington's disease
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在位置辨别和逆转任务中由喹啉酸损伤纹状体引起的缺陷可以通过苍白球的永久性和暂时性损伤来改善：亨廷顿病大鼠模型的潜在新疗法
DOI：
10.1002/mds.10622
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发表时间：
2003
影响因子：
8.6
通讯作者：
I. Weiner
中科院分区：
文献类型：
--
作者：
D. Joel;L. Ayalon;R. Tarrasch;I. Weiner
亨廷顿病（HD）早期的症状被认为反映了基底神经节回路功能障碍，继发于苍白球外段的纹状体投射变性（GPe）。 GPe 损伤将通过使回路功能“正常化”来改善 HD 症状的假设已在该疾病的大鼠模型中进行了测试。将喹啉酸损伤纹状体的大鼠（HD大鼠模型）在位置辨别和逆转任务中的表现与在纹状体损伤同时（实验1）或纹状体损伤后1个月（实验2）同时进行的双侧苍白球（GP）兴奋性毒性损伤以及纹状体损伤后1个月（实验2）以及单侧苍白球暂时性损伤的大鼠的表现进行比较。 GP（实验3）。通过同时或纹状体损伤后 1 个月进行的双侧兴奋毒性 GP 损伤以及暂时的单侧 GP 失活，可以有效逆转纹状体损伤引起的任务缺陷。鉴于基底神经节回路的类似功能障碍被认为会促进喹啉酸损伤大鼠的行为改变和 HD 的一些症状，这些结果提出了 GPe 的损伤或失活可能减轻 HD 某些症状的可能性。 © 2003 运动障碍协会
Symptoms in the early stages of Huntington's disease (HD) are assumed to reflect basal ganglia circuit dysfunction secondary to degeneration of striatal projections to the external segment of the globus pallidus (GPe). The hypothesis that GPe lesion would ameliorate HD symptoms by “normalizing” the circuit's functioning was tested in a rat model of this disease. The performance of rats sustaining quinolinic acid lesion to the striatum (a rat model of HD) in a position discrimination and reversal task was compared with the performance of rats sustaining in addition a bilateral excitotoxic lesion to the globus pallidus (GP) carried out simultaneously with the striatal lesion (Experiment 1) or 1 month after the striatal lesion (Experiment 2), as well as a unilateral temporary lesion of the GP (Experiment 3). The striatal lesion‐induced deficit in the task was effectively reversed by a bilateral excitotoxic GP lesion carried out simultaneously or 1 month after the striatal lesion, as well as by a temporary unilateral GP inactivation. Given that a similar dysfunction of basal ganglia circuitry is thought to subserve the behavioral alterations seen in quinolinic acid lesioned rats and some of the symptoms in HD, these results raise the possibility that lesion or inactivation of the GPe may alleviate some of HD symptoms. © 2003 Movement Disorder Society
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DOI：
10.1073/pnas.85.15.5733
发表时间：
1988-08-01
影响因子：
11.1
作者：
REINER, A;ALBIN, RL;YOUNG, AB
通讯作者：
YOUNG, AB
亨廷顿病中强直和舞蹈症的神经化学底物。
DOI：
10.1093/brain/116.5.1201
发表时间：
1993
期刊：
Brain : a journal of neurology
影响因子：
--
作者：
Storey,E;Beal,MF
通讯作者：
Beal,MF
DOI：
10.1056/nejm198611133152006
发表时间：
1986-11
期刊：
The New England journal of medicine
影响因子：
--
作者：
J. B. Martin;J. Gusella
通讯作者：
J. B. Martin;J. Gusella
影响因子：
2.5
作者：
MINK, JW;THACH, WT
通讯作者：
THACH, WT
猴子苍白球局部失活期间手臂位置、运动和丘脑放电控制的变化。
DOI：
10.1152/jn.1996.75.3.1087
发表时间：
1996
期刊：
Journal of neurophysiology.
影响因子：
--
作者：
Inase,M;Buford,JA;Anderson,ME
通讯作者：
Anderson,ME