Neural Systems of Ingestive Behavior

描述(申请人提供)：肥胖的发生是因为个人经常摄入的卡路里比他们消耗的更多。当食物的奖励价值大于肠道中产生的饱腹感信号的总和时，就会发生这种情况。然而，赋予味觉享乐性价值的神经机制仍然未知。决定是否摄取或拒绝食物的神经基础在脑干中完成。在大鼠的脑干中，含有味觉和迷走神经内脏传入系统的第一和第二中枢中继器，负责摄食行为的运动神经元，以及做出这一决定的足够的综合能力。然而，控制摄取需要连接到前脑和从前脑连接，因为切断前脑与脑干的连接会消除自愿进食。总而言之，这项研究的目标是了解前脑如何与这些后脑机制相互作用，实现对进食行为的平稳、细微的控制，这是老鼠和人类等杂食动物的特征。利用行为学、神经解剖学、神经化学和电生理学分析，这个项目将测试有关味觉刺激的奖赏价值如何在大脑中阐述的假说。第一个目标是进一步确定臂旁核的特定腹侧前脑投射，这些投射对于调节多巴胺的释放至关重要，因为它是味觉刺激的奖赏(和厌恶)特性的函数。目的2通过比较伏隔核和杏仁中央核--前脑奖赏系统中假定的节点--在稳态和享乐性摄取过程中的多巴胺释放，说明这些联系的功能相关性。目的3研究不同口感刺激和口后刺激时桥脑味觉传输器的味觉神经活动。这些发现将有助于理解基本的调控机制，这些机制无法控制易患饮食肥胖的个人的摄入量，因为现代饮食的适口性增加带来的刺激增加。 与公共健康相关：美味的食物会刺激超出生理需要的摄入量，这是一种导致肥胖的效应。为了了解这种享乐式进食的感觉整合，我们将检测口服蔗糖刺激时的味觉神经反应和中枢多巴胺释放。这个项目将帮助我们确定正常的良好调节行为，如饮食，如何会偏离到导致流行病的地步。

DESCRIPTION (provided by applicant): Obesity occurs because individuals regularly ingest more calories than they expend. This takes place when the reward value of the food is greater than the sum of the satiety signals arising in the gut. Nevertheless, the neural mechanisms that assign hedonic value to taste remain unknown. The neural substrates for the decision to whether ingest or reject a food are complete in the brainstem. In rats, the brainstem contains the first and second central relays for both the gustatory and vagal visceral afferent systems, the motoneurons responsible for ingestive behavior, and sufficient integrative capacity to make this decision. Nevertheless, control of ingestion requires connections to and from the forebrain because disconnecting it from the brainstem eliminates voluntary eating. Writ large, the goal of this research is to understand how the forebrain interacts with these hindbrain mechanisms to bring about the smooth, nuanced control of feeding behavior that characterizes omnivores such as rats and humans. Using behavioral, neuroanatomical, neurochemical, and electrophysiological analysis, this project will test hypotheses about how the reward value of gustatory stimuli is elaborated in the brain. The first Aim is to further determine the specific ventral forebrain projections from the parabrachial nuclei that are critical for modulating dopamine release as a function of the rewarding (and aversive) properties of taste stimuli. Aim 2 addresses functional correlates of those connections by comparing dopamine release in the nucleus accumbens and the central nucleus of the amygdala -- putative nodes in the forebrain reward system -- during homeostatic and hedonic ingestion. Aim 3 focuses on gustatory neural activity in the pontine taste relays while varying both oral and postoral taste stimulation. The findings will aid in understanding basic regulatory mechanisms that fail to control intake in individuals susceptible to developing dietary obesity due to increased stimulation from augmented palatability of the modern diet. PUBLIC HEALTH RELEVANCE: Palatable foods stimulate intake beyond physiological needs, an effect that leads to obesity. To understand the sensory integration responsible for such hedonic eating, we will examine gustatory neural responses and central dopamine release during oral sucrose stimulation. This project will help us determine how a normally well regulated behavior, such as eating, can go so far awry as to cause an epidemic.