BIOLOGICAL MECHANISMS OF THE ANTIDEPRESSANT EFFECTS OF SLEEP DEPRIVATION

完全睡眠剥夺一晚导致60例患者暂时缓解 重度抑郁症患者的百分比：它还可以诱发躁狂症， 躁郁症患者 此外，一小时的睡眠也会引发 抑郁症患者在睡眠剥夺后有所改善。 因此，在本发明中， 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。 这个项目的目的 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， 可能会导致新的，快速激活的药物治疗， 抑郁和躁狂 目前的项目旨在验证一个假设 体温调节机制是 睡眠和睡眠剥夺。 这个假设是基于我们的观察 睡眠的许多生理反应类似于 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），并抑制代谢 产热和促甲状腺激素（TSH和三碘甲状腺原氨酸）分泌 （T3）。 与寒冷暴露一样，睡眠剥夺也有相反的效果。 我们 测试睡眠的热样性质和睡眠的热样性质的假设， 睡眠剥夺的冷样属性是他们的临床负责 和神经内分泌的影响。 根据该 假设，与凉爽环境相比，温暖的环境应该 减弱睡眠剥夺的抗抑郁和神经内分泌作用。 患者有一次在33 ℃的环境温度下被剥夺睡眠 在另一个场合，在18度的环境温度下 C.已经对12名患者进行了研究，结果与 假设。 睡眠剥夺后在凉爽条件下比较 与温暖的条件下，抗抑郁作用更大（P <0.05）， 促甲状腺激素分泌的增加更大（p <0.05）， T3的增加更大（p <0.01），PRL的抑制 大于（p小于0.03）。 结果表明 睡眠的神经内分泌效应可以被热模拟 exposure.

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.