课题基金 / 基金详情

HOMEOSTATIC ORIGINS OF MOTIVATION

HOMEOSTATIC ORIGINS OF MOTIVATION
动机的稳态起源
批准号:
2033558
负责人:
EDWARD M STRICKER
金额:
$25.92万
依托单位国家:
美国
项目类别:
财政年份:
1979
资助国家:
美国
项目状态:
已结题
起止时间:
1979-06-01 至 2001-05-31

项目摘要

项目成果

EDWARD M STRICKER的其他基金

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中文摘要
翻译
描述(改编自申请人的摘要):这是一个竞争性的 一般目的是 了解动机行为的生物学基础,特别是口渴, 盐食欲,饥饿和饱腹感。 提出了两个系列的实验 阐明摄食行为的中枢机制, 控制。 实验1的目的是确定脑干机制, 哪些胃信号会影响正在进行的摄入。 为了实现这一目标, 实验1A确定了手术损伤核的大鼠是否 孤束核(NTS)口渴时会过度饮水,10%蔗糖 饥饿时用0.3 M NaCl溶液,有盐食欲时用0.3 M NaCl, 将在饮用测试的前10-15分钟内这样做;实验1B 确定全身注射胆囊收缩素(CCK)是否会抑制 食物摄入和刺激NTS损伤大鼠垂体OT分泌, 就像在邻近最后区(AP)损伤的大鼠和 实验1C确定是否适度胃扩张 能增强CCK对AP大鼠的减食欲作用, NTS和对照组大鼠;实验1D确定CCK是否 预处理将消除AP损伤大鼠的过度饮酒, 对实验1A中提到的各种饮酒刺激的反应。 实验2旨在确定中央回路的组织 调节口渴和NaCl食欲。 为了实现这一目标,实验2A 决定了脑室内脑损伤的影响, 施用与OT缀合的植物细胞毒素蓖麻毒素(rA-OT),或 心房钠尿肽(rA-ANP),治疗损害的功能, 脑细胞轴承OT或心钠素受体,分别对渗透压和 低血容量诱导的水和NaCl溶液的摄入;实验2B 分析rA-OT和rA-ANP对细胞和功能回路的损伤 实验2C确定了刺激表达的脑细胞 高渗NaCl溶液与等渗高渗溶液的cFos比较 实验2D定位受刺激表达cFos的细胞 用高渗氯化钠溶液对rA-ANP诱导的大鼠脑损伤进行治疗。
英文摘要
DESCRIPTION (Adapted from applicant's abstract): This is a competing renewal application for grant support of research whose general goal is to understand the biological bases of motivated behavior, especially thirst, salt appetite, hunger and satiety. Two series of experiments are proposed to elucidate the central mechanisms by which ingestive behavior is controlled. Experiment 1 aims to determine the brain stem mechanisms by which gastric signals affect ongoing ingestion. In pursuit of this aim, Experiment 1A determines whether rats with surgical lesions of nucleus tractus solitarius (NTS) will overdrink water when thirsty, 10% sucrose solution when hungry, and 0.3 M NaCl when they have a salt appetite, and will do so in the first 10-15 min of the drinking test; Experiment 1B determines whether systemic injection of cholecystokinin (CCK) will inhibit food intake and stimulate pituitary OT secretion in rats with NTS lesions, as it does in rats with lesions of the adjacent area postrema (AP) and in control rats; Experiment 1C determines whether moderate gastric distension will potentiate the anorectic effect of CCK in rats with lesions of AP or NTS and in control rats; and Experiment 1D determines whether CCK pretreatment will eliminate the overdrinking of rats with AP lesions in response to the various stimuli for drinking mentioned in Experiment 1A. Experiment 2 aims to determine the organization of central circuits mediating thirst and NaCl appetite. In pursuit of this aim, Experiment 2A determines the effect of brain lesions produced by intracerebroventricular administration of the plant cytotoxin ricin conjugated to OT (rA-OT) or atrial natriuretic peptide (rA-ANP), treatments which impair the function of brain cells bearing OT or ANP receptors, respectively, on osmotic- and hypovolemia-induced ingestion of water and NaCl solution; Experiment 2B analyzes the cells and functional circuits damaged by rA-OT and rA-ANP treatments; Experiment 2C identifies the brain cells stimulated to express cFos by hypertonic NaCl solution compared to equiosmolar hypertonic mannitol; and Experiment 2D localizes the cells stimulated to express cFos by hypertonic NaC1 solution in rats with rA-ANP induced brain lesions.
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