NEURAL REGULATION OF VASOPRESSIN RELEASE

描述(来自应用程序的逐字)：加压素是主要的 荷尔蒙参与体液动态平衡。它是由神经元分泌的 在下丘脑视上核(SON)和室旁核(PVN)。 血压、血容量和血浆渗透压的变化影响 兴奋特定中枢神经系统对SON和PVN内加压素神经元的激活作用 小路。后叶加压素神经元介导这些效应的通路 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给 那只老鼠。对参与调控的中枢神经系统通路知之甚少 心脏受体对SON神经元活性的影响。所描述的实验 在这项提案中将研究神经通路使动脉 压力感受器信息和心脏感受器信息传递给儿子。首先，我们 将确定CNS中因容量扩展而激活的区域 Fos免疫细胞化学和WE法在非麻醉大鼠等渗盐水中的应用 将决定心脏受体在激活这些细胞中的作用 地区。这些研究得出的数据将被用作 我们获得细胞外的活体电生理实验 麻醉大鼠加压素和催产素SON神经元的记录。在……里面 这些研究，我们将直接刺激心脏受体来确定它们 对SON神经元活动的影响。中确定的CNS区域的作用 FOS实验将被测试它们在 SON神经元对心脏受体刺激的电生理反应 通过给它们注射一种名为鹅膏藤酸的兴奋毒素。我们的初步结果 指出两个重要的发现。首先，可能会有相当大的重叠 动脉压力感受器和心脏感受器之间的通路 把信息传给儿子。其次，心脏受体的激活可能 差异调节加压素和催产素神经元的活动 儿子。最近，加压素释放的非渗透调节的变化 与终末期心脏循环中高水平的加压素有关 故障和在太空飞行期间观察到的细胞外液容量的变化以及 长期卧床休息(诺斯克，1996)。对加压素释放的控制也是 在怀孕期间发生了变化。在我们能够解决加压素是如何 在这些状态下释放会发生变化，我们需要确定神经 加压素非渗透调节机制的研究进展 分泌物。因此，了解神经通路参与了 动脉压力感受器和心房感受器对加压素释放的调节 这是必要的第一步，需要解决后叶加压素的作用 健康和疾病。

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.