Distribution of Transglutaminase 6 in the Central Nervous System of Adult Mice

Distribution of Transglutaminase 6 in the Central Nervous System of Adult Mice
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转谷氨酰胺酶6在成年小鼠中枢神经系统中的分布

DOI:
10.1002/ar.22741
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发表时间:
2013-10-01
影响因子:
2
通讯作者:
Wang, Jun-Ling
Wang, Jun-Ling
中科院分区:
医学4区
文献类型:
--
作者:
Liu, Yu-Tao;Tang, Bei-Sha;Wang, Jun-Ling

文献摘要

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我们以前的研究发现了一种新的脊髓小脑共济失调(SCA),其中编码转氨酶6(TG 6)的基因突变被认为是致病原因。然而,关于TG 6在脑中的细胞分布的数据仍然是零碎的。因此,我们现在报告一个全面的免疫组织化学检查成年小鼠大脑中的TG 6的表达谱。TG 6在隔区、基底节、下丘脑和脑干中表达丰富。值得注意的是,在参与调节运动活动的关键大脑区域中发现了许多TG 6阳性神经元,包括苍白球,丘脑底核,黑质,小脑,一些小脑前核和脊髓运动神经元。双重免疫染色显示,网状黑质中的绝大多数TG 6阳性神经元是GABA能神经元,而致密黑质中的TG 6阳性神经元不是多巴胺能神经元。此外,用抗NeuN或胶质细胞酸性蛋白(GFAP)抗体对TG 6进行双重染色,证明了NeuN-TG 6的排他性共定位。本研究全面概述了TG 6在小鼠脑中的表达,并为研究TG 6在SCA发展中的作用提供了见解。Anat Rec,296:1576-1587,2013.© 2013 Wiley Periodicals,Inc.
Our previous study identified a new form of spinocerebellar ataxia (SCA), in which mutations in the gene coding for transglutaminase 6 (TG6) were suggested to be causative. However, the data concerning cellular distribution of TG6 in the brain is still fragmentary. Therefore, we now report a comprehensive immunohistochemical examination of the expression profile of TG6 in adult mouse brain. TG6 was abundantly expressed in the septal region, basal ganglia, hypothalamus and brainstem. Notably, numerous TG6‐positive neurons were found in the key brain regions involved in regulating locomotion activity, including the globus pallidus, subthalamic nucleus, substantia nigra, cerebellum, some precerebellar nuclei, and spinal motor neurons. Double immunostaining showed that the vast majority of TG6‐positive neurons in the reticular nigra were GABAergic and those in the compact nigra were not dopaminergic. In addition, double staining for TG6 with either anti‐NeuN or glial fibrillary acidic protein (GFAP) antibodies demonstrated exclusive NeuN‐TG6 co‐localization. This study presents a comprehensive overview of TG6 expression in the mouse brain, and provides insight for investigating the role of TG6 in the development of SCA. Anat Rec, 296:1576–1587, 2013. © 2013 Wiley Periodicals, Inc.