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NEURAL REGULATION OF VASOPRESSIN RELEASE

NEURAL REGULATION OF VASOPRESSIN RELEASE
加压素释放的神经调节
批准号:
6390356
负责人:
J Thomas Cunningham
金额:
$18.13万
依托单位国家:
美国
项目类别:
财政年份:
2000
资助国家:
美国
项目状态:
已结题
起止时间:
2000-09-15 至 2005-08-31

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中文摘要
翻译
描述(来自应用程序的逐字):加压素是主要的 与体液平衡有关的激素。它是由位于 下丘脑视上核(SON)和室旁核(PVN)。 血压、血容量和血浆渗透压的变化影响 通过激活特定的CNS,SON和PVN中的加压素神经元的活性 途径。介导血管加压素神经元这些作用的通路在脑内是不稳定的。 儿子还没有被完全描述。我们以前研究过中枢神经系统通路 参与将信息从动脉压力感受器传递到 老鼠对参与调节的中枢神经系统通路知之甚少 SON神经元活动的心脏感受器。描述的实验 在这项提案中,将研究神经通路, 压力感受器信息和心脏感受器信息。一是 将识别CNS中由体积扩张激活的区域, 用Fos免疫细胞化学和免疫组织化学方法, 将决定心脏受体在这些激活中的作用 地区从这些研究中获得的数据将用作 体内电生理实验中,我们获得细胞外 来自麻醉大鼠中的加压素和催产素SON神经元的记录。在 在这些研究中,我们将直接刺激心脏受体,以确定它们的 影响SON神经元的活动。中枢神经系统区域的作用, Fos实验的重要性将在 视上核神经元对心脏感受器刺激的电生理反应 用一种叫鹅膏蕈氨酸的兴奋性毒素破坏它们我们的初步结果 显示了两个重要发现。第一,可能有相当大的重叠 动脉压力感受器和心脏感受器之间的通路 儿子的信息。其次,心脏受体的激活可能 差异调节血管加压素和催产素神经元的活性, 儿子最近,加压素释放的非渗透调节的改变, 与晚期心脏血管加压素的高循环水平有关 失败和变化的细胞外液量观察到在太空飞行和 长期卧床休息(Norsk,1996)。加压素释放的控制也是 在怀孕期间改变。在我们讨论加压素 在这些状态下,释放发生了变化,我们需要确定神经 参与加压素非渗透控制的机制 分泌物因此,了解参与的神经通路, 动脉压力感受器和心房感受器调节加压素的释放, 这是解决后叶加压素在 健康和疾病。
英文摘要
DESCRIPTION (Verbatim from the application): Vasopressin is one of the major hormones involved in body fluid homeostasis. It is secreted by neurons located in the supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamus. Changes in blood pressure, blood volume and plasma osmolality influence the activity of vasopressin neurons in the SON and PVN by activating specific CNS pathways. The pathways that mediate these effects of vasopressin neurons in the SON have not been fully described. We have previously studied the CNS pathways involved in transmitting information from arterial baroreceptors to the SON of the rat. Much less is known about the CNS pathways involved in the regulation of the activity of SON neurons by cardiac receptors. The experiments described in this proposal will examine the neural pathways that bring arterial baroreceptor information and cardiac receptor information to the SON. First, we will identify the areas in the CNS that are activated by volume expansion with isotonic saline in unanesthetized rats using Fos immunocytochemistry and we will determine the role of cardiac receptors in the activation of these regions. The data resulting from these studies will be used as the basis for in vivo electrophysiological experiments in which we obtain extracellular recordings from vasopressin and oxytocin SON neurons in anesthetized rats. In these studies, we will directly stimulate cardiac receptors to determine their influence on the activity of SON neurons. The role of CNS regions identified in the Fos experiments will be tested for their importance in the electrophysiological responses of SON neurons to cardiac receptor stimulation by lesioning them with an excitotoxin, ibotenic acid. Our preliminary results indicate two important findings. First, there may be considerable overlap between the pathways bringing arterial baroreceptor and cardiac receptor information to the SON. Second, the activation of cardiac receptors may differentially regulate the activity of vasopressin and oxytocin neurons in the SON. Recently, alterations in the non-osmotic regulation of vasopressin release have been linked to high circulating levels of vasopressin in end stage heart failure and to changes in extracellular fluid volume observed during space flight and prolonged bed rest (Norsk, 1996). The control of vasopressin release is also altered during pregnancy. Before we can address how vasopressin release is changed during these states, we need to determine the neural mechanisms that participate in the non-osmotic control of vasopressin secretion. Therefore, understanding the neural pathways involved in the arterial baroreceptor and atrial receptor regulation of vasopressin release is a necessary first step that is needed to address the role of vasopressin in health and disease.
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