AFFERENT SIGNALING AND FOREBRAIN MECHANISMS IN THE BEHAVIORAL-CONTROL OF EXTRACELLULAR FLUID VOLUME
AFFERENT SIGNALING AND FOREBRAIN MECHANISMS IN THE BEHAVIORAL-CONTROL OF EXTRACELLULAR FLUID VOLUME
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DOI：
10.1111/j.1749-6632.1993.tb55545.x
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发表时间：
1993-07-22
影响因子：
5.2
通讯作者：
JOHNSON, AK
中科院分区：
文献类型：
--
作者：
ZARDETTOSMITH, AM;THUNHORST, RL;JOHNSON, AK
身体通过激活自主神经和内分泌反射以及动员行为机制来防御细胞外液量减少。纠正细胞外液缺乏所需的行为涉及水和钠的摄入。可以合理地假设，来自动脉和心肺高压和容量受体的传入神经输入，以及 ANG II 形式的传入体液输入，是重要的系统生成信号，充当细胞外耗竭引起的口渴和钠食欲的传入介质。来自这些信号的神经信息已被证明会聚在位于终板的前脑结构上，在该结构上可能会发生这种输入的处理和整合。本文描述了对伴随快速诱导钠食欲的传入信号传导机制的分析。由于与肾素-血管紧张素系统活性升高相结合的容量和压力相关输入可能对于产生这种形式的诱导高渗氯化钠和水摄入很重要，因此我们重点关注终板的结构，特别是 SFO、MnPO 和 OVLT。采用免疫细胞化学方法检测早期癌基因 c-fos 的研究表明，终板神经元以及 SON 和 PVN 被产生口渴和钠食欲所必需的系统衍生信号复合物激活。到目前为止，我们还没有彻底了解这些内脏信号如何激活这些动机行为的神经基础。然而，这些研究结合了功能和神经解剖学方法，为研究维持体液平衡和心血管稳态的行为和生理控制系统的神经生物学基础提供了策略。本文描述了对伴随快速诱导钠食欲的传入信号传导机制的分析。由于与容量和压力相关的输入，以及肾素-血管紧张素系统活性的升高，可能对于产生这种形式的诱导高渗氯化钠和水摄入很重要，因此我们重点关注终板的结构，特别是 SFO、MnPO 和 OVLT。采用免疫细胞化学方法检测早期癌基因 c-fos 的研究表明，终板神经元以及 SON 和 PVN 被产生口渴和钠食欲所必需的系统衍生信号复合物激活。到目前为止，对于这些内脏感觉相关信号如何激活这些动机行为的神经基质还没有透彻的了解。（摘要截断为 400 字）
The body defends against reduced extracellular fluid volume both by activation of autonomic and endocrine reflexes and by mobilization of behavioral mechanisms. The behaviors that are required to correct an extracellular fluid deficit involve the ingestion of both water and sodium. It is reasonable to hypothesize that afferent neural input from both arterial and cardiopulmonary high pressure and volume receptors, and afferent humoral input in the form of ANG II, are important systemically-generated signals acting as afferent mediators of extracellular depletion-induced thirst and sodium appetite. Neural information from these signals has been shown to converge on forebrain structures located along the lamina terminalis where processing and integration of this input is likely to take place. This paper describes an analysis of the mechanisms of afferent signaling that accompanies a form of rapidly induced sodium appetite. Because volume and pressure-related input in concert with elevated activity of the renin-angiotensin system is likely to be important for generating this form of induced hypertonic sodium chloride and water intake, we have focused on the structures of the lamina terminalis, specifically the SFO, MnPO, and OVLT. Investigations that employ immunocytochemical methods for the detection of the early oncogene, c-fos, indicate that neurons in the lamina terminalis, as well as the SON and PVN, are activated by the composite of systemically derived signals necessary for producing thirst and sodium appetite. So far, there is no thorough understanding of how these visceral signals activate the neural substrates for these motivated behaviors. However, these studies, combining both functional and neuroanatomical approaches, provide a strategy for investigating the neurobiological basis of the behavioral and physiological control systems that maintain fluid balance and cardiovascular homeostasis. This paper describes an analysis of the mechanisms of afferent signaling that accompanies a form of rapidly induced sodium appetite. Because volume and pressure-related input, in concert with elevated activity of the renin-angiotensin system, is likely to be important for generating this form of induced hypertonic sodium chloride and water intake, we have focused on the structures of the lamina terminalis, specifically the SFO, MnPO, and OVLT. Investigations that employ immunocytochemical methods for the detection of the early oncogene, c-fos, indicate that neurons in the lamina terminalis, as well as the SON and PVN, are activated by the composite of systemically derived signals necessary for producing thirst and sodium appetite. So far, there is no thorough understanding of how these visceral sensory-related signals activate the neural substrates for these motivated behaviors.(ABSTRACT TRUNCATED AT 400 WORDS)