CYTOKINE AND ENDOCRINE SLEEP REGULATION

白细胞介素-1（IL-1）、肿瘤坏死因子（TNF）和生长激素 非快速眼动睡眠中释放激素（GHRH）增加 （NREMS）。 本提案的目的是增进我们对以下问题的了解： 细胞因子/内分泌在睡眠调节中的作用。 我们假设 睡眠因子（SF）IL-1、TNF和GHRH介导NREMS反应， 睡眠剥夺、感染和结核病。 大量数据表明IL-1、TNF 和GHRH在NREMS监管，例如，外源性IL-1、TNF或GHRH增强 几个物种的NREMS。 初步数据也支持这一假设， 例如，在一个实施例中，睡眠剥夺后的NREMS反弹减弱，如果动物 用抗IL-1、抗TNF或抗GHRH预处理。 具体目标是 本研究拟通过测定血中IL-1、TNF和GHRH水平， 和特定的大脑区域后，睡眠剥夺，注射 微生物产物和Tamb的轻度增加。 据预测 在每次操作后，推定的SF水平将增加。 的 结果将影响这些SF是否用于生理学 睡眠调节的作用。 目前，我们既不知道它的功能， 睡眠的细胞和分子机制的 睡眠的分子原因的知识可能是一个必要的 进一步了解睡眠功能。 拟议研究 将提供有关正常睡眠调节的信息， 睡眠障碍，细胞因子/旁分泌调节机制， 神经系统和免疫系统之间的相互作用。

Interleukin-1 (IL-1), tumor necrosis factor (TNF), and growth hormone releasing-hormone (GHRH) increase in non-rapid eye movement sleep (NREMS). The objective of this proposal is to advance our knowledge of the role cytokines/endocrines play in sleep regulation. We hypothesize that sleep factor (SF) IL-1, TNF and GHRH mediate NREMS responses to sleep deprivation, infection and T amb. Much data implicate IL-1, TNF and GHRH in NREMS regulation, e.g., exogenous IL-1, TNF or GHRH enhances NREMS in several species. Preliminary data also support this hypothesis, e.g., NREMS rebound after sleep deprivation is attenuated if animals are pretreated with anti-IL-1, anti-TNF or anti-GHRH. The specific aim of this proposal is to determine the levels of IL-1, TNF and GHRH in blood and specific brain regions after sleep deprivation, injection of microbial products and mild increases in Tamb. It is predicted that the levels of the putative SF will increase after each manipulation. The results will have a bearing on whether these SFs serve a physiological role in sleep regulation. At present, we know neither the functions, nor the exact cellular and molecular mechanisms responsible for sleep. The knowledge of the molecular causes of sleep is likely to be a necessary step toward our understanding of sleep function. The proposed research will provide information concerning normal sleep regulation, a variety of sleep disorders, cytokine/paracrine regulator mechanism, and interactions between the nervous and immune systems.