HOMEOSTATIC ORIGINS OF MOTIVATION

这是一项与之竞争的继续申请赠款支持的申请 其总体目标是了解生物学基础的研究 有动机的行为，特别是口渴、食盐、饥饿 和饱腹感，以及补充生理上的贡献 动态平衡。激励的概念指的是 寻找、获取和消费食物或饮料。这是传统的 将需求视为这种冲动的基础。钠的食欲和 口渴确实反映了这种需要；在这两种情况下，都是兴奋刺激 似乎促进了摄取，而抑制刺激则终止了它。在……里面 相比之下，对于食物摄入量，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。近期 研究表明，催产素能神经元的活动 从室旁核(PVN)向中央投射， 反映在脑下后叶催产素(OT)的分泌中，与 抑制大鼠进食和摄取氯化钠。六个系列 有人提议用实验来检验这一假说。的作用 几种肠肽荷尔蒙，包括缩胆囊素， 蛙皮素和胰岛素在抑制大鼠的食物摄取中是 实验1的重点。胃胀可能是另一个原因 这方面的重要抑制刺激，以及实验1 还检测了不同剂量的丹参对大鼠胃排空的影响。 已知的治疗方法可以减少食物摄入量。的影响 破坏室旁核或去甲肾上腺素能和5-羟色胺能传入 对PVN，对大鼠恶心反应中OT分泌的影响 代理是实验2的焦点。实验3检查了 中枢加压素能神经元在食物控制中的作用 人体摄入量。实验4确定是否 催产素分泌的诱导改变与不同种类的 已知的影响老鼠摄取氯化钠的治疗方法。实验5 确定在不同的大鼠钠摄取模型中， 盐胁迫对OT分泌的刺激作用减弱。 实验6A考察了海藻糖对钠摄取的影响。 破坏PVN或PVN的单胺能传入。最后， 实验6B考察了控制食物和食物的交互作用 通过测定大鼠食盐摄入对恶心的影响- 关于钠食欲的生产制剂和假定的饱腹剂， 渗透压刺激对OT分泌和摄食量的影响。

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.