SENSORY AND HORMONAL CONTROL OF SALT APPETITE

对盐食欲过程中味觉加工的研究， 聚焦两个假设。第一个假设是， 味觉的神经编码被改变， 钠对动物更重要。第二个假设是 腹侧前脑中的亲和力改变的机制， 在中央味觉系统之外，在神经系统内， 这些变化是由控制体液平衡的激素改变的。 第一个假设需要行为和电生理学 实验钠食欲可以引起各种各样的 所有这些都导致盐摄入量增加。是什么 目前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发生了同样的变化。我们 计划使用两个短期措施，味觉反应测试和 舔模式分析，以确定是否行为 在钠饥饿期间对味觉的反应不同， 提高食欲的方法。 这些行为 这些实验部分是由电生理学数据引起的， 这表明饮食中钠的缺乏会降低 利尿剂增加中枢味觉神经对NaCl的反应。 这些数据表明，不同的程序引发一个 食欲对有味道的钠产生不同的知觉改变。 对这些现象的进一步分析， 进一步在臂旁核（PBN）的中央被指示。 双侧PBN病变消除了钠的表达 食欲在幼稚大鼠，但类似的病变，无论是在核 孤束或丘脑味觉传递的神经元则没有。 PBN中的味觉神经元不仅投射到丘脑， 腹侧前脑也是根据损伤的结果 研究，从脑桥到腹侧的味觉投射 前脑的重要性更大 第二个假设的研究将集中在神经元内的 视隔-视前区连续体， 离子电渗应用的血管紧张素。这种神经元的数量 在那些 已经用DOCA进行了预处理。事实上， 整个地区的安全都得到了DOCA的加强。在下一个项目中 在此期间，将作出大量努力，审查 这种类固醇作用的范围和机制。单独意见 已经证明，在某些地方， 离子电渗施用的血管紧张素可升高血压， 甚至诱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改变， DOCA预处理。

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.