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在特发性肌张力障碍仓鼠模型的肌张力障碍发作期间,外侧缰核中c-fos表达异常。

Abnormal c-fos expression in the lateral habenula during dystonic attacks in a hamster model of idiopathic dystonia.

作者信息

Ebert U, Gernert M, Löscher W, Richter A

机构信息

Department of Pharmacology, Toxicology and Pharmacy, School of Veterinary Medicine, Hannover, Germany.

出版信息

Brain Res. 1996 Jul 22;728(1):125-9.

PMID:8864307
Abstract

The genetically dystonic hamster (dtsz), an animal model of idiopathic dystonia, displays sustained twisting movements and postures either spontaneously or in response to mild stress. In the present study the expression of c-fos immunoreactive neurons (Fos-ir), used as an indicator of neuronal activity, was investigated within various brain regions in dtsz hamsters and non-dystonic control hamsters. Under baseline condition, i.e. in the absence of dystonia, the expression of Fos-ir did not reveal any differences between dtsz hamsters and controls. However, in response to mild stress several brain regions, particularly the lateral habenula (LHb), exhibited differences in c-fos induction in dtsz hamsters and controls. Whereas in the LHb the expression of Fos-ir was markedly enhanced in controls, it showed almost no increase in dystonic hamsters, indicating impaired neuronal activity. Since the lateral habenula receives major input from the basal ganglia via the entopeduncular nucleus, the present data might indicate that basal ganglia are involved in the dystonic syndrome in mutant hamsters.

摘要

遗传性肌张力障碍仓鼠(dtsz)是特发性肌张力障碍的一种动物模型,会自发地或在受到轻度应激时出现持续的扭转运动和姿势。在本研究中,作为神经元活动指标的c-fos免疫反应性神经元(Fos-ir)在dtsz仓鼠和非肌张力障碍对照仓鼠的各个脑区中的表达情况得到了研究。在基线条件下,即不存在肌张力障碍时,dtsz仓鼠和对照仓鼠之间Fos-ir的表达没有显示出任何差异。然而,在受到轻度应激时,几个脑区,特别是外侧缰核(LHb),在dtsz仓鼠和对照仓鼠中c-fos的诱导表现出差异。在对照仓鼠的LHb中,Fos-ir的表达明显增强,而在肌张力障碍仓鼠中几乎没有增加,这表明神经元活动受损。由于外侧缰核通过内苍白球核从基底神经节接收主要输入,目前的数据可能表明基底神经节参与了突变仓鼠的肌张力障碍综合征。

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Deficit of striatal parvalbumin-reactive GABAergic interneurons and decreased basal ganglia output in a genetic rodent model of idiopathic paroxysmal dystonia.在特发性阵发性肌张力障碍的遗传性啮齿动物模型中,纹状体小白蛋白反应性γ-氨基丁酸能中间神经元缺失及基底神经节输出减少。
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