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迷走神经损伤后大鼠延髓中27 kDa热休克蛋白(Hsp27)的诱导表达。

Induction of the 27-kDa heat shock protein (Hsp27) in the rat medulla oblongata after vagus nerve injury.

作者信息

Hopkins D A, Plumier J C, Currie R W

机构信息

Department of Anatomy and Neurobiology, Dalhousie University, Halifax, Nova Scota, B3H 4H7, Canada.

出版信息

Exp Neurol. 1998 Oct;153(2):173-83. doi: 10.1006/exnr.1998.6870.

DOI:10.1006/exnr.1998.6870
PMID:9784277
Abstract

The 27-kDa heat shock protein (Hsp27) is constitutively expressed in motor and sensory neurons of the brainstem. Hsp27 is also rapidly induced in the nervous system following oxidative and cellular metabolic stress. In this study, we examined the distribution of Hsp27 in the rat medulla oblongata by means of immunohistochemistry after the vagus nerve was cut or crushed. After vagal injury, rats were allowed to survive for 6, 12, 24 h, 2, 4, 7, 10, 14, 30, or 90 days. Vagus nerve lesions resulted in a time-dependent up-regulation of Hsp27 in vagal motor and nodose ganglion sensory neurons that expressed Hsp27 constitutively and de novo induction in neurons that did not express Hsp27 constitutively. In the dorsal motor nucleus of the vagus nerve (DMV) and nucleus ambiguus, the levels of Hsp27 in motor neurons were elevated within 24 h of injury and persisted for up to 90 days. Vagal afferents to the nucleus of the tractus solitarius (NTS) and area postrema showed increases in Hsp27 levels within 4 days that were still present 90 days postinjury. In addition, increases in Hsp27 staining of axons in the NTS and DMV suggest that vagus nerve injury resulted in sprouting of afferent axons and spread into areas of the dorsal vagal complex not normally innervated by the vagus. Our observations are consistent with the possibility that Hsp27 plays a role in long-term survival of distinct subpopulations of injured vagal motor and sensory neurons.

摘要

27 kDa热休克蛋白(Hsp27)在脑干的运动和感觉神经元中组成性表达。在氧化和细胞代谢应激后,Hsp27也会在神经系统中迅速被诱导产生。在本研究中,我们通过免疫组织化学方法,在切断或挤压迷走神经后,检测了大鼠延髓中Hsp27的分布情况。迷走神经损伤后,让大鼠存活6、12、24小时、2、4、7、10、14、30或90天。迷走神经损伤导致迷走运动神经元和结状神经节感觉神经元中Hsp27呈时间依赖性上调,这些神经元原本组成性表达Hsp27,而在原本不组成性表达Hsp27的神经元中则出现了从头诱导。在迷走神经背运动核(DMV)和疑核中,运动神经元内的Hsp27水平在损伤后24小时内升高,并持续长达90天。孤束核(NTS)和最后区的迷走传入神经中,Hsp27水平在4天内升高,损伤后90天仍存在。此外,NTS和DMV中轴突的Hsp27染色增加表明,迷走神经损伤导致传入轴突发芽,并扩散到通常不由迷走神经支配的迷走背侧复合体区域。我们的观察结果与Hsp27在受损迷走运动和感觉神经元不同亚群的长期存活中发挥作用的可能性一致。

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