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: 3880941
• 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/3880941
• 关键词: bipolar depression manic phase; body temperature regulation; hormone metabolism; hormone regulation /control mechanism; human subject; major depression; neuroendocrine system; prolactin; psychobiology; sleep deprivation; somatotropin; sweat; thyrotropin; triiodothyronine

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 two hours 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 biological 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 acting 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 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, compared with a cool environment, should blunt the antidepressant and neuroendocrine effects of sleep deprivation. Patents and normal individuals are sleep-deprived on one occasion in an ambient temperature of 90 degrees F, and on another occasion in an ambient temperature of 62 degrees F. In twelve patients studied so far, the results are consistent with the predictions based on our hypothesis, but some additional subjects are needed to permit definitive statistical evaluation of the insults.

完全睡眠剥夺一晚导致60例患者暂时缓解 %的重度抑郁症患者;它也可以诱发躁狂症， 躁郁症患者此外，仅仅两个小时的睡眠就可以触发 抑郁症患者在睡眠剥夺后有所改善。因此 睡眠似乎有一种兴奋的效果，而清醒则是一种情绪提升 效果这些观察对管理层有实际意义 情感性疾病例如，一些患者的抑郁症可能是 睡眠剥夺治疗，睡眠中断有时是一种 可识别和可预防躁狂症的原因。本项目的目的是 试图找出抗抑郁作用的生物学机制 睡眠不足的症状生物学机制的确定将 增加对抑郁症和躁狂症发病机制的了解， 有望带来新的、快速起效的药物治疗， 抑郁和躁狂 目前的项目旨在测试一个假设，即体温调节 睡眠改变情绪的机制 剥夺这个假设是基于我们的观察， 对睡眠的生理反应类似于对热暴露的反应。像 热暴露，睡眠开始刺激分泌汗液，催乳素（PRL） 和生长激素（GH），它抑制代谢产热， 分泌TSH和三碘甲状腺原氨酸（T3）。比如冷暴露，睡眠 剥夺会产生相反的效果。我们正在验证一个假设， 睡眠的类热性和睡眠剥夺的类冷性 对抑郁症的临床和神经内分泌影响负有责任 患者根据这一假设，与一个温暖的环境相比， 凉爽的环境，应钝化抗抑郁药和神经内分泌 睡眠剥夺的影响。专利和普通人 有一次在90华氏度的环境温度下被剥夺了睡眠， 而在另一个场合在62华氏度的环境温度下。在 到目前为止，研究了12名患者，结果与 预测基于我们的假设，但一些额外的主题是 需要允许明确的统计评估的侮辱。