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年轻和中年雌性 Sprague-Dawley 大鼠特定脑区中类固醇受体共激活因子-1(SRC-1)免疫反应性的改变。

Alterations of steroid receptor coactivator-1 (SRC-1) immunoreactivities in specific brain regions of young and middle-aged female Sprague-Dawley rats.

机构信息

Department of Neurobiology, Chongqing Key Laboratory of Neurobiology, Third Military Medical University, Chongqing 400038, China.

出版信息

Brain Res. 2011 Mar 25;1382:88-97. doi: 10.1016/j.brainres.2011.01.024. Epub 2011 Jan 15.

Abstract

Previous studies have shown that steroid receptor coactivator-1 (SRC-1) is involved in the regulation of Purkinje cell development and motor learning, neural stem cell differentiation and reproductive-related plasticity. It is widely distributed in the adult brain, but the aging-related changes in the brain remain unclear. In this study age-related alterations of SRC-1 expression in female brain were examined. The results showed that striking age-related decreases of SRC-1 were noticed in those regions related to central regulation of motor (substantia nigra, pontine nuclei, lateral reticular nucleus and Purkinje cells, etc.), learning and memory (olfactory bulb, hippocampus, Purkinje cells, etc.), and neural stem cell (olfactory, dentate gyrus, cerebral cortex, etc.). Surprisingly, although SRC-1 immunopositive materials were predominantly detected in the cell nuclei, they were also detected in the extra-nuclear components predominantly in these motor-regulation sub-regions. The above results showing age-related decrease of SRC-1 in specific motor, learning and memory nuclei suggested its potential roles in neurodegenerative disorders, which may be one of the underlying mechanisms of the vulnerability of the aged brain.

摘要

先前的研究表明,类固醇受体共激活因子-1(SRC-1)参与调节浦肯野细胞发育和运动学习、神经干细胞分化和与生殖相关的可塑性。它广泛分布于成年大脑中,但大脑与年龄相关的变化尚不清楚。在这项研究中,研究了女性大脑中 SRC-1 表达与年龄相关的变化。结果表明,在与运动(黑质、脑桥核、外侧网状核和浦肯野细胞等)、学习和记忆(嗅球、海马、浦肯野细胞等)以及神经干细胞(嗅球、齿状回、大脑皮层等)相关的中枢调节相关区域中,SRC-1 的表达显著随年龄增长而减少。令人惊讶的是,尽管 SRC-1 免疫阳性物质主要在细胞核中检测到,但在这些运动调节亚区的核外成分中也主要检测到了它们。上述结果表明,SRC-1 在特定的运动、学习和记忆核中的表达随年龄的增长而减少,这表明其在神经退行性疾病中具有潜在作用,这可能是老年大脑易感性的潜在机制之一。

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