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首页> 外文期刊>The European Journal of Neuroscience >The effect of air puff stress on c-Fos expression in rat hypothalamus and brainstem: Central circuitry mediating sympathoexcitation and baroreflex resetting
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The effect of air puff stress on c-Fos expression in rat hypothalamus and brainstem: Central circuitry mediating sympathoexcitation and baroreflex resetting

机译：吹气压力对大鼠下丘脑和脑干c-Fos表达的影响：介导交感神经兴奋和压力感受反射复位的中央回路

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摘要

Psychological stress evokes increases in sympathetic activity and blood pressure, which are due at least in part to an upward resetting of the baroreceptor-sympathetic reflex. In this study we determined whether sympathetic premotor neurons in the rostral ventrolateral medulla (RVLM), which have a critical role in the reflex control of sympathetic activity, are activated during air puff stress, a moderate psychological stressor. Secondly, we identified neurons that are activated by air puff stress and that also project to the nucleus tractus solitarius (NTS), a key site for modulation of the baroreceptor reflex. Air puff stress resulted in increased c-Fos expression in several hypothalamic and brainstem nuclei, including the paraventricular nucleus (PVN), dorsomedial hypothalamus, perifornical area (PeF), periaqueductal gray (PAG), NTS and rostral ventromedial medulla, but not in the RVLM region that contains sympathetic premotor neurons. In contrast, neurons in this RVLM region, including catecholamine-synthesizing neurons, did express c-Fos following induced hypotension, which reflexly activates RVLM sympathetic premotor neurons. The highest proportion of NTS-projecting neurons that were double-labelled with c-Fos after air puff stress was in the ventrolateral PAG (29.3 ± 5.5%), with smaller but still significant proportions of double-labelled NTS-projecting neurons in the PVN and PeF (6.5 ± 1.8 and 6.4 ± 1.7%, respectively). The results suggest that the increased sympathetic activity during psychological stress is not driven primarily by RVLM sympathetic premotor neurons, and that neurons in the PVN, PeF and ventrolateral PAG may contribute to the resetting of the baroreceptor-sympathetic reflex that is associated with psychological stress.
机译：心理压力引起交感神经活动和血压升高，这至少部分是由于压力感受器交感神经反射的向上复位所致。在这项研究中，我们确定了在吹气压力（一种中等的心理压力源）期间，在交感神经活动反射控制中起关键作用的延髓腹侧延髓（RVLM）中的交感神经运动前神经元是否被激活。其次，我们确定了由吹气压力激活的神经元，并且也投射到孤束核（NTS），它是压力感受器反射调节的关键部位。吹气压力会导致下丘脑和脑干核中c-Fos表达的增加，包括心室旁核（PVN），丘脑下丘脑，腹膜周区域（PeF），导水管周围灰质（PAG），NTS和延髓腹侧延髓，但并非如此RVLM区域包含交感神经运动前神经元。相反，该RVLM区域中的神经元（包括儿茶酚胺合成神经元）在诱导的低血压后确实表达c-Fos，从而反射性激活RVLM交感性运动前神经元。在气喘压力后以c-Fos双重标记的NTS投射神经元比例最高的是腹侧PAG（29.3±5.5％），而在PVN中以双重标记的NTS投射神经元比例较小但仍很重要和PeF（分别为6.5±1.8和6.4±1.7％）。结果表明，心理应激期间交感神经活动的增加并非主要由RVLM交感神经运动前神经元驱动，PVN，PeF和腹侧PAG中的神经元可能会导致与心理应激相关的压力感受器-交感神经反射的复位。

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