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窦主动脉去神经支配对清醒家兔高血压和低血压诱发的脑内Fos表达的影响。

Effects of sinoaortic denervation on Fos expression in the brain evoked by hypertension and hypotension in conscious rabbits.

作者信息

Potts P D, Polson J W, Hirooka Y, Dampney R A

机构信息

Department of Physiology, University of Sydney, New South Wales, Australia.

出版信息

Neuroscience. 1997 Mar;77(2):503-20. doi: 10.1016/s0306-4522(96)00459-9.

Abstract

We have previously shown [Li and Dampney (1994) Neuroscience 61, 613-634] that periods of sustained hypertension and hypotension each induces a distinctive and reproducible pattern of neuronal expression of Fos (a marker of neuronal activation) in specific regions of the brainstem and forebrain of conscious rabbits. The aim of this study was to determine the contribution of afferent inputs from arterial baroreceptors to the activation of neurons in these various brain regions that is caused by a sustained change in arterial pressure. Experiments were carried out on rabbits in which the carotid sinus and aortic depressor nerves were cut in a preliminary operation. Following a recovery period of seven to 10 days, a moderate hypertension or hypotension (increase or decrease in arterial pressure of 20-30 mmHg) was induced in conscious barodenervated rabbits for 60 min by the continuous infusion of phenylephrine or sodium nitroprusside, respectively. In control experiments, barodenervated rabbits were subjected to the identical procedures except that they were infused with the vehicle solution alone. Compared with the effects seen in barointact rabbits, [Li and Dampney (1994) Neuroscience 61, 613-634] the number of neurons that expressed Fos in response to hypertension was reduced by approximately 90% in the nucleus of the solitary tract and in the caudal and intermediate parts of the ventrolateral medulla. In supramedullary regions, baroreceptor denervation resulted in a reduction of approximately 60% in hypertension-induced Fos expression in the central nucleus of the amygdala and in the bed nucleus of the stria terminalis, but no significant reduction in the parabrachial complex in the pons. Following hypotension, the number of neurons that expressed Fos in barodenervated rabbits, compared with barointact rabbits, [Li and Dampney (1994) Neuroscience 61, 613-634] was reduced by approximately 90% in the nucleus of the solitary tract, area postrema, and caudal, intermediate and rostral parts of the ventrolateral medulla. Baroreceptor denervation also resulted in a similar large reduction in hypotension-induced Fos expression in many supramedullary regions (locus coeruleus, midbrain periaqueductal grey, hypothalamic paraventricular nucleus, and in the central nucleus of the amygdala and the bed nucleus of the stria terminalis in the basal forebrain). In the supraoptic nucleus, hypotension-induced Fos expression in barodenervated rabbits was reduced by 75% compared to barointact animals, but was still significantly greater than in control animals. There was also a high level of Fos expression, much greater than in control animals, in the circumventricular organs surrounding the third ventricle (subfornical organ and organum vasculosum lamina terminalis). The results indicate that in conscious rabbits the activation of neurons that occurs in several discrete regions at all levels of the brain following a sustained change in arterial pressure is largely dependent upon inputs from arterial baroreceptors, with the exception of neurons in the circumventricular organs surrounding the third ventricle that are activated by sustained hypotension. The latter group of neurons are known to project to vasopressin-secreting neurons in the supraoptic nucleus, and may therefore via this pathway trigger the hypotension-induced release of vasopressin that occurs in the absence of baroreceptor inputs.

摘要

我们之前已经表明[Li和Dampney(1994年),《神经科学》61卷,613 - 634页],持续性高血压和低血压阶段分别在清醒兔子的脑干和前脑特定区域诱导出一种独特且可重复的Fos神经元表达模式(Fos是神经元激活的标志物)。本研究的目的是确定来自动脉压力感受器的传入输入对这些因动脉压持续变化而被激活的不同脑区神经元的激活所起的作用。实验在兔子身上进行,在初步手术中切断其颈动脉窦和主动脉减压神经。经过7至10天的恢复期后,分别通过持续输注去氧肾上腺素或硝普钠,在清醒的去神经支配兔子中诱导出中度高血压或低血压(动脉压升高或降低20 - 30 mmHg),持续60分钟。在对照实验中,去神经支配兔子接受相同的操作,但仅输注溶剂溶液。与在完整压力感受器兔子中观察到的效应相比[Li和Dampney(1994年),《神经科学》61卷,613 - 634页],在延髓孤束核以及腹外侧延髓的尾部和中间部分,因高血压而表达Fos的神经元数量减少了约90%。在延髓以上区域,压力感受器去神经支配导致杏仁核中央核和终纹床核中高血压诱导的Fos表达减少约60%,但在脑桥臂旁复合体中无显著减少。在低血压后,与完整压力感受器兔子相比,去神经支配兔子中在延髓孤束核、最后区以及腹外侧延髓的尾部、中间和嘴侧部分表达Fos的神经元数量减少了约90%。压力感受器去神经支配还导致许多延髓以上区域(蓝斑、中脑导水管周围灰质、下丘脑室旁核以及基底前脑的杏仁核中央核和终纹床核)中低血压诱导的Fos表达出现类似的大幅减少。在视上核中,与完整压力感受器动物相比,去神经支配兔子中低血压诱导的Fos表达减少了75%,但仍显著高于对照动物。在围绕第三脑室的室周器官(穹窿下器官和终板血管器)中也有高水平的Fos表达,远高于对照动物。结果表明,在清醒兔子中,动脉压持续变化后在脑的所有水平的几个离散区域中发生的神经元激活在很大程度上依赖于来自动脉压力感受器的输入,但第三脑室周围室周器官中因持续性低血压而被激活的神经元除外。后一组神经元已知投射到视上核中分泌血管加压素的神经元,因此可能通过这条途径触发在没有压力感受器输入时发生的低血压诱导的血管加压素释放。

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