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孤束核儿茶酚胺能神经元调节大鼠对应激的心血管反应。

Nucleus of the solitary tract catecholaminergic neurons modulate the cardiovascular response to psychological stress in rats.

机构信息

Ferris State University, Department of Biological Sciences, Big Rapids, MI 49307, USA.

出版信息

J Physiol. 2012 Oct 1;590(19):4881-95. doi: 10.1113/jphysiol.2012.232314. Epub 2012 Jul 2.

DOI:10.1113/jphysiol.2012.232314
PMID:22753543
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3487043/
Abstract

Catecholaminergic neurons within the central nervous system are an integral part of stress-related neurocircuitry, and the nucleus of the solitary tract (NTS) plays a critical role in cardiovascular regulation. We tested the hypothesis that NTS catecholaminergic neurons attenuate psychological stress-induced increases in blood pressure and promote neuroendocrine activation in response to psychological stress.Anti-dopamine-β-hydroxylase antibody conjugated to the neurotoxin saporin (DSAP) or saline vehicle was microinjected into the NTS to lesion catecholaminergic neurons in male Sprague-Dawley rats, and 17 days later the rats were subjected to 60 min of restraint stress for five consecutive days. DSAP treatment significantly enhanced the integrated increase in mean arterial pressure during restraint on the first (800 ± 128 and 1115 ± 116 mmHg (min) for saline- and DSAP-treated rats) and fifth days (655 ± 116 and 1035 ± 113 mmHg (min) for saline- and DSAP-treated rats; P<0.01 for overall effect of DSAP treatment) of restraint. In contrast, after 60 min of restraint plasma corticosterone concentration was significantly lower in DSAP-treated compared with saline-treated rats (25.9 ± 7 compared with 46.8 ± 7 μg dl(-1) for DSAP- and saline-treated rats; P <0.05). DSAP treatment also significantly reduced baseline plasma adrenaline concentration (403 ± 69 compared with 73 ± 29 pg ml(-1) for saline- and DSAP-treated rats), but did not alter the magnitude of the adrenaline response to restraint. The data suggest that NTS catecholaminergic neurons normally inhibit the arterial pressure response, but help maintain the corticosterone response to restraint stress.

摘要

中枢神经系统中的儿茶酚胺能神经元是应激相关神经回路的一个组成部分,而孤束核(NTS)在心血管调节中起着关键作用。我们假设 NTS 儿茶酚胺能神经元减弱心理应激引起的血压升高,并促进神经内分泌激活以应对心理应激。

将与神经毒素相思豆毒素(DSAP)结合的抗多巴胺-β-羟化酶抗体或生理盐水载体注入 NTS 以损伤雄性 Sprague-Dawley 大鼠的儿茶酚胺能神经元,17 天后,大鼠连续 5 天接受 60 分钟的束缚应激。DSAP 处理显著增强了束缚期间平均动脉压的综合增加,在第一天(盐水和 DSAP 处理的大鼠分别为 800 ± 128 和 1115 ± 116mmHg(min))和第五天(盐水和 DSAP 处理的大鼠分别为 655 ± 116 和 1035 ± 113mmHg(min))。相比之下,束缚 60 分钟后,DSAP 处理的大鼠血浆皮质酮浓度明显低于盐水处理的大鼠(DSAP 和盐水处理的大鼠分别为 25.9 ± 7 和 46.8 ± 7μg dl(-1);P<0.05)。DSAP 处理还显著降低了基础血浆肾上腺素浓度(盐水和 DSAP 处理的大鼠分别为 403 ± 69 和 73 ± 29pg ml(-1)),但不改变肾上腺素对束缚的反应幅度。数据表明,NTS 儿茶酚胺能神经元通常抑制动脉压反应,但有助于维持皮质酮对束缚应激的反应。

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