HOMEOSTATIC ORIGINS OF MOTIVATION

这是一个竞争性的继续申请， 以了解生物学基础为总目标的研究 有动机的行为，特别是口渴，钠的食欲，饥饿 和饱腹感，以及互补的生理贡献， 体内平衡 动机的概念是指 寻找、获取和消费食物或饮料。 传统上， 把需求作为这种冲动的基础。 钠食欲和 口渴确实反映了这种需要;在这两种情况下， 似乎促进摄入和抑制性刺激终止它。 相反，对于食物摄入，我们关注的是抑制性刺激， 因为特定的兴奋性刺激似乎不存在。 最近 研究表明催产素能神经元的活动 从室旁核（PVN）中央突出， 反映在垂体催产素（OT）分泌，与 抑制大鼠的食物和NaCl摄入。 六大系列 提出实验来检验这一假设。 的作用 几种肠肽激素，包括胆囊收缩素， 蛙皮素和胰岛素在抑制大鼠摄食中的作用是 实验1的焦点。 胃扩张可能是另一个原因 在这方面重要的抑制刺激，和实验1 还检查了不同剂量的药物对大鼠胃排空的影响。 已知的减少食物摄入的治疗方法。 的影响 破坏PVN或去甲肾上腺素能和肾上腺素能传入神经 PVN对恶心大鼠OT分泌的影响 实验2的重点是人工智能。 实验3考察了 中枢加压素能神经元在食物控制中的作用 摄入人体受试者。 实验4确定是否 诱导的OT分泌的改变平行于各种 已知影响大鼠NaCl摄入的治疗。 实验5 确定在大鼠的各种钠食欲模型中， NaCl消耗对OT分泌的刺激减弱。 实验6A检查了以下物质对钠食欲的影响： 破坏PVN或PVN的单胺能传入。 最后， 实验6 B检查了食物和药物对照中的相互作用。 通过测定恶心的影响， 产生剂和假定的饱腹感剂对钠食欲的影响， 以及渗透压刺激对OT分泌的影响。

This is a competing continuation application for grant support of research whose general goal is to understand the biological bases of motivated behavior, especially thirst, sodium appetite, hunger and satiety, and the complementary physioligcal contributions to homeostasis. The concept of motivation refers to the urge to seek, obtain and consume food or drink. It is traditional to consider need as the basis for this urge. Sodium appetite and thirst do reflect such a need; in both cases excitratory stimuli seem to promote ingestion and inhibitory stimuli terminate it. In contrast, with food intake we are focsussing on inhibitory stimuli because specific excitartroy stimuli do not seem to exist. Recent research has suggested that activity in oxytocinergic neurons projecting centrally from the paraventricular necleus (PVN), reflected in pituitary oxytocin (OT) secretion, associated with the inhibition of food and NaCl ingestion in rats. Six series of experiments are proposed to test this hypothesis. The role of several enteric peptide hormones, including cholecytokinin, bombesin, and insulin, in the inhibition of food intake in rats is the focus of Experiment 1. Gastric distention may be another important inhibitory stimulus in this regard, and Experiment 1 also examines the effects on gastric emptying in rats of various treatments known to reduce food intake. The effects of destroying PVN, or the noradrenergic and serotonergic afferents to PVN, on OT secretion of rats in response to nausea-producing agents is the focus of Experiment 2. Experiment 3 examines the role of the central vasopressinergic neurons in the control of food intake in human subjects. Experiment 4 determines whether induced alterations in OT secretion parallel the effects of various treatments known to affect NaCl ingestion in rats. Experiment 5 determines whether in various models of sodium appetite in rats, the stimulation of OT secretion by NaCl consumption is blunted. Experiment 6A examines the effects on sodium appetite of destroying PVN, or the monoaminergic afferents to PVN. Finally, Experiment 6B examines interactions in the controls of food and NaCl ingestion in rats by determining the effects of nausea- producing agents and putative satiety agents on sodium appetite, and the effects of osmotic stimuli to OT secretion on food intake.