SENSORY AND HORMONAL CONTROL OF SALT APPETITE

食盐期间味觉加工的研究将 重点关注两个假设。第一个假设是感官 味觉的神经编码以一种方式改变，使口头 钠对动物的影响更大。第二种假设是 腹侧前脑亲和力改变的机制， 超越中枢味觉系统，在神经系统内 它们被控制液体平衡的荷尔蒙改变。 第一种假设需要行为学和电生理学 实验。可以用各种不同的食物来引起食欲 程序，所有这些都会导致盐摄入量增加。是什么 尚不清楚盐摄入量的类似变化是否反映了 对钠离子的享乐反应也有同样的变化。我们 计划使用两种短期措施，味觉反应性测试和 舔舔模式分析，以确定是否有行为 钠饥饿时对味觉的反应因以下因素而不同 用来提高食欲的方法。这些行为 实验在一定程度上是由电生理数据推动的 证明饮食中的缺钠减少，而 利尿剂可增加中枢味觉神经对氯化钠的反应。 这些数据表明，不同的程序可以引发 食欲会对皂化钠产生不同的知觉变化。 对外围和外围这些现象的进一步分析 在臂旁核(PBN)的更中央是支配的。 双侧PBN病变消除钠的表达 幼稚大鼠的食欲，但类似的损害要么在细胞核 孤束或丘脑味觉传递不起作用。 PBN中的味觉神经元不仅投射到丘脑，而且 腹侧的前脑也是如此。从损伤的结果来看 研究表明，从脑桥到腹侧的味觉投射 前脑具有额外的重要性。 对第二种假设的研究将集中在大脑中的神经元。 视前隔-视前连续体选择性地对 离子导入应用血管紧张素。这样的神经元的数量 在动物身上，它们的反应强度会增加 已经用DOCA进行了预处理。事实上，自发的活动 通过DOCA加强了整个区域的可持续发展。在下一个项目中 在此期间，将致力于研究 这种类固醇效应的范围和机制。单独的观察 已经证明，在某些地点，微量的 血管紧张素应用于离子导入可升高血压和 甚至会引发饮酒行为。我们还将确定PBN是否 对该区域神经元的影响可以选择性地用 DOCA前处理。

Investigations of gustatory processing during salt appetite will focus on two hypotheses. The first hypothesis is that the sensory neural code for taste is altered in a manner that makes oral sodium more salient to the animal. The second hypothesis places the mechanism for the changed avidity in the ventral forebrain, beyond the central gustatory system, within the neural systems that are altered by the hormones controlling fluid balance. The first hypothesis requires behavioral and electrophysiological experiments. Na-appetite can be elicited with variety of procedures, all of which result in increased salt intake. What is not clear is whether a similar change in salt intake reflects the same alterations in the hedonic response to the sodium ion. We plan to use two short term measures, the taste reactivity test and lick pattern analysis, to determine whether the behavioral responses to taste during sodium hunger differ as a function of the method used to raise the appetite. These behavioral experiments were prompted, in part, by electrophysiological data demonstrating that dietary sodium deprivation reduces while diuretics increase central gustatory neural response to NaCl. These data suggest that different procedures for eliciting an appetite produce different perceptual alterations to sapid sodium. Further analysis of these phenomena both on the periphery and further centrally in the parabrachial nuclei (PBN) is dictated. Bilateral lesions of the PBN eliminate the expression of sodium appetite in naive rats, but similar lesions either in the nucleus of the solitary tract or the thalamic gustatory relay do not. Gustatory neurons in the PBN project not only to thalamus, but also to the ventral forebrain. Given the results from the lesion studies, the gustatory projections from the pons to the ventral forebrain take on added significance. Studies of the second hypothesis will focus on neurons within the septo-preoptic continuum that respond selectively to iontophoretically applied angiotensin. The number of such neurons and the magnitude of their responses increases in animals that have been pretreated with DOCA. In fact, the spontaneous activity of the entire region is enhanced by DOCA. During the next project period, a substantial effort will be devoted to examining the range and mechanisms of this steroid effect. Separate observations have demonstrated that, at some locations, minute doses of angiotensin applied iontophoretically can raise blood pressure and even elicit drinking behavior. We also will determine whether PBN influence on neurons in the area can be altered selectively with DOCA pretreatment.