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。了解它的神经基础是发展理性的关键 治疗一系列疾病的方法，如药物成瘾、肥胖、 神经性厌食症和抑郁症。食盐是一种由生物引发的动力 通过负的身体钠平衡为研究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的 动机的标准，就像饥渴一样，但有一些明显的 优势。它的足够刺激很简单，钠离子，在 外部环境，这种刺激是由一个单一的感觉系统传递的， 品尝一下。与其他感官系统不同，除了嗅觉，味觉有直接的神经 与边缘系统的联系，这对阐述 动力。在大多数哺乳动物中，包括人类，对钠的识别是与生俱来的。 因此，当食欲升高时，感觉神经的意义 皂化钠引发的活性发生了巨大的变化。这样做的目的是 该项目是为了了解控制食盐量的神经系统是如何 影响对盐的亲和力的变化。前提是至少有一部分 变化是由味觉神经编码的改变引起的。我们已经知道了 在钠摄取过程中，对氯化钠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 区域(NST)。我们还知道第二个中央中继器的损伤， 臂旁核(PBN)可抑制Na-胃纳的表达，但 对第三个中央中继区丘脑味觉区域(TTA)的损害则不会。 最后，对NST和PBN都完好无损的大鼠进行慢性去大脑， 但没有与前脑的联系，也不能表现出 纳氏胃口。这些事实限制了假设仅限于 臂旁核和边缘系统。使用这些约束，本提案检查 三个相关的假设。在纳食欲期间，(1)感觉神经编码 PBN中的味道被改变，使皂化钠更容易与其他 化学物质，(2)臂旁味觉神经活动分布到 腹侧前脑是改变大脑的享乐性价值的充分必要条件 盐信号，以及(3)提高辨别能力和 亲和力的改变涉及边缘系统之间的相互作用 还有臂旁核。

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.