Gustatory Control of Sodium Appetite

描述（由申请人提供）：动机仍然是一个核心难题， 神经科学理解它的神经基础是发展理性思维的关键 治疗多种疾病，如药物成瘾，肥胖， 神经性厌食症和抑郁症。盐的食欲是一种生物驱动， 负钠平衡提供了一个独特的模型， 动机行为的核心机制。钠的胃口满足了所有 动机的标准，如饥饿和口渴，但有一些不同的 优势它的足够刺激是简单的，钠离子，并在 外部环境，这种刺激是由一个单一的感觉系统， 味道与其他感觉系统不同，除了嗅觉，味觉有直接的神经系统。 与边缘系统的联系，这是至关重要的阐述 动机在大多数哺乳动物中，包括人类，对钠的识别是天生的。 因此，当一个Na-食欲出现时，感觉神经的重要性 由sapid钠引起的活性显著变化。的目的 该项目旨在了解控制盐食欲的神经系统 影响对盐的亲和力的变化。前提是，至少部分 味觉神经编码的改变导致了这种变化。我们已经知道 在钠食欲期间，对NaCl的味觉反应确实发生了变化 在外围和第一个中央继电器中，孤束核 束（NST）。我们还知道，第二个中央中继的病变， 臂旁核（PBN），阻止Na-食欲的表达，但 第三个中枢中继--丘脑味觉区（TTA）的损伤则不会。 最后，慢性去脑大鼠，其NST和PBN均完整， 但没有连接到或从前脑，也没有表现出 没胃口这些事实将假设限制在 PBN和边缘系统。利用这些限制因素，本提案审查了 三个相关假设在Na食欲期间，（1）感觉神经代码 PBN中的味道被改变，使咸味钠与其他咸味钠更易区分。 化学物质，（2）臂旁味觉神经活动分布到 腹侧前脑是必要的，足以改变享乐价值的 盐信号，和（3）增加的辨别力的机制， 改变的亲和力涉及边缘系统之间的相互作用， 和臂旁核

DESCRIPTION (provided by applicant): Motivation remains a central puzzle of neuroscience. Understanding its neural bases is key in developing rational therapies for a broad spectrum of maladies such as drug addiction, obesity, anorexia nervosa, and depression. Salt appetite is a biological drive triggered by a negative body sodium balance that offers a unique model for investigating the central mechanisms of motivated behavior. Sodium appetite fulfills all of the criteria for motivation, as do hunger and thirst, but has some distinct advantages. Its adequate stimulus is simple, the sodium ion, and in the external environment, this stimulus is transduced by a single sensory system, taste. Unlike other sensory systems, except smell, taste has direct neural connections with the limbic system, which is critical to the elaboration of motivation. In most mammals, including humans, recognition of sodium is innate. Thus, when a Na-appetite arises, the significance of the sensory neural activity elicited by sapid sodium changes dramatically. The objective of this project is to understand how the neural systems that control salt appetite effect the change in avidity for salt. The premise is that at least part of the change results from alterations in the gustatory neural code. We already know that, during Na-appetite, changes do occur in the gustatory responses to NaCl on the periphery and in the first central relay, the nucleus of the solitary tract (NST). We also know that lesions of the second central relay, the parabrachial nucleus (PBN), prevent the expression of Na-appetite, but that damage to the third central relay, the thalamic gustatory area (TTA), does not. Finally, chronically decerebrate rats, which have both the NST and PBN intact, but no connections to or from the forebrain, also fail to exhibit a Na-appetite. These facts constrain the hypotheses to interactions between the PBN and the limbic system. Using these constraints, this proposal examines three related hypotheses. During Na-appetite, (1) the sensory neural code for taste in the PBN is altered to make sapid sodium more discriminable from other chemicals, (2) parabrachial gustatory neural activity distributed to the ventral forebrain is necessary and sufficient to change the hedonic value of the salt signal, and (3) the mechanism for the increased discriminability and the changed avidity involves reciprocal interaction between the limbic system and the parabrachial nuclei.