Orexin-1 receptor expression after global ischemia in mice

Orexin-1 receptor expression after global ischemia in mice
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DOI:
10.1016/j.regpep.2004.08.037
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发表时间:
2005-03-15
影响因子:
--
通讯作者:
Shioda, SJ
Shioda, SJ
中科院分区:
其他
文献类型:
--
作者:
Nakamachi, T;Endo, S;Shioda, SJ

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食欲素是具有一系列生理作用的神经肽,包括摄食行为和睡眠-觉醒周期的调节。近年来,我们报道了一些神经退行性疾病患者脊髓液中食欲素A水平降低,认为食欲素A及其受体可能与中枢神经系统疾病有关。然而,食欲素受体的表达和定位并没有被很好地诱导。因此,本研究旨在通过免疫组织化学技术研究短暂性颈总动脉闭塞(tCCAO)后小鼠脑内食欲素受体(OX 1 R)的变化及其随时间的变化。OX 1 R的免疫反应显着增加,并在海马和皮质tCCAO后2天达到高峰,但在下丘脑保持不变。使用双重免疫组化,OX 1 R免疫阳性细胞在tCCAO后2天共定位不仅与神经元标记,NeuN-免疫反应,但也与星形胶质细胞和少突胶质细胞标记,GFAP-和CNPase-immunoreactivity,分别。提示OX 1 R在缺血应激过程中除神经元外还可被其它细胞诱导表达,食欲素及其受体可能在缺血损伤中起重要作用。(C)2004 Elsevier B. V.保留所有权利。
Orexins are neuropeptides that have a range of physiological effects including die regulation of feeding behavior and the sleep-wakefulness cycle. Recently, we reported that level of orexin A in spinal fluid was decreased in the patients of some neurodegenerative diseases and it is considered that orexin A and the receptors might be related to central nervous system disorders. However, the expression and localization of orexin receptors is not elicited well. Therefore, the purpose of this study is to investigate the time-dependent changes, and the cellular localization of orexin receptor focusing on orexin-1 receptor (OX1R) in the mouse brain after transient common carotid artery occlusion (tCCAO) model by using immunohistochemical techniques. OX1R immunoreactivity dramatically increased and peaked in the hippocampus and cortex 2 day after tCCAO, but remained unchanged in the hypothalamus. Using double-immunohistochemistry, the OX1R immunopositive cells at 2 days after tCCAO were co-localized not only with neuronal marker, NeuN-immunoreactivity but also with astroglial and oligodendroglial markers, GFAP- and CNPase-immunoreactivities, respectively. These results suggested that OX1R is induced other cells in addition to the neurons during stress such as ischemia and orexins and its receptor might play an important role for ischemic insult. (C) 2004 Elsevier B.V. All rights reserved.