BIOLOGICAL MECHANISMS OF THE ANTIDEPRESSANT EFFECTS OF SLEEP DEPRIVATION

睡眠剥夺抗抑郁作用的生物学机制

• 批准号: 3845263
• 负责人: T A WEHR
• 金额: --
• 依托单位: NATIONAL INSTITUTE OF MENTAL HEALTH
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/3845263
• 关键词: bipolar depression manic phase; body temperature regulation; cold temperature; heat; hormone regulation /control mechanism; human subject; major depression; neuroendocrine system; phototherapy; prolactin; seasonal affective disorder; sleep deprivation; somatotropin; sweat; thyrotropin; triiodothyronine; wakefulness

Total sleep deprivation for one night induces temporary remissions in sixty percent of patients with major depression: it can also induce mania in bipolar patients. Furthermore, as little as one hour of sleep can trigger depression in patients who have improved after sleep deprivation. Thus, sleep appears to have a depressant effect and wakefulness a mood-elevating effect. These observations have practical implications for the management of affective illness. For example, some patients' depressions can be treated with sleep deprivation, and sleep disruption is sometimes an identifiable and preventable cause of mania. The purpose of this project is to attempt to identify biology mechanisms of the antidepressant effects of sleep deprivation. Identification of biological mechanisms would increase understanding of the pathogenesis of depression and mania and could be expected to lead to new, rapidly activing drug treatments for depression and mania. The current project is designed to test a hypothesis that thermoregulatory mechanisms underlie the mood-altering effects of sleep and sleep deprivation. The hypothesis is based on our observation that many of the physiological responses to sleep resemble responses to heat exposure. Like heat exposure, sleep onset stimulates secretion of sweat, prolactin (PRL) and growth hormone (GH), and it inhibits metabolic heat production and secretion of thyrotropin (TSH and triiodothyronine (T3). Like cold exposure, sleep deprivation has opposite effects. We are testing the hypothesis that the heat-like property of sleep and the cold-like property of sleep deprivation are responsible for their clinical and neuroendocrine effects in depressed patients. According to this hypothesis, a warm environment, compare with a cool environment, should blunt the antidepressant and neuroendocrine effects of sleep deprivation. Patients are sleep-deprived on one occasion in an ambient temperature of 33 degrees C, and on another occasion in an ambient temperature of 18 degrees C. Twelve patients have been studied, and the results are consistent with the hypothesis. After sleep deprivation in the cool condition compared with the warm condition antidepressant effects were greater (p less than 0.03) augmentation of TSH secretion was greater (p less than 0.05), augmentation of T3 was greater (p less than 0.01), and suppression of PRL was greater (p equals less than 0.03). The results show that the depressant and neuroendocrine effects of sleep can be mimicked by heat exposure.

完全睡眠不足一晚会导致60%的人暂时缓解 患有严重抑郁症的患者比例：它还可以在 躁郁症患者。此外，只需一小时的睡眠就可以触发 睡眠剥夺后改善的患者的抑郁。因此， 睡眠似乎有抑制情绪的作用，而清醒则能提升情绪。 效果。这些观察结果对管理层具有实际意义。 情感上的疾病。例如，一些患者的抑郁可能是 接受睡眠剥夺治疗，睡眠中断有时是一种 躁狂症的可识别和可预防的原因。这个项目的目的是 就是试图确定抗抑郁作用的生物学机制 睡眠不足。生物机制的识别将 加深对抑郁症和躁狂症发病机制的认识 有望带来新的、迅速活跃的药物治疗方法 抑郁和狂躁。目前的项目旨在检验一个假说 体温调节机制是改变情绪的效果的基础 睡眠和睡眠剥夺。这一假设是基于我们的观察得出的 对睡眠的许多生理反应类似于对睡眠的反应 热暴露。像热暴露一样，睡眠开始刺激分泌 汗液、催乳素(PRL)和生长激素(GH) 促甲状腺激素(TSH和三碘甲腺原氨酸)的产热和分泌 (T3)。与寒冷暴露一样，睡眠不足也会产生相反的效果。我们是 检验这样一种假设，即睡眠的类热属性和 睡眠剥夺的冷样性质是导致其临床症状的原因 以及抑郁症患者的神经内分泌效应。根据这一点 假设，温暖的环境与凉爽的环境相比，应该 削弱睡眠剥夺对抗抑郁剂和神经内分泌的影响。 患者有一次在33度的环境温度下睡眠不足 摄氏度，还有一次是在18摄氏度的环境温度下 C.对12名患者进行了研究，结果与 假设。睡眠剥夺后在凉爽状态下的比较 在温暖条件下，抗抑郁作用更强(p< 0.03)TSH分泌增加幅度较大(p<0.05)， T_3升高较大(P<0.01)，PRL则受到抑制 大于(p等于小于0.03)。结果表明， 高温可以模拟睡眠的抑郁和神经内分泌作用 曝光。