REM SLEEP DEPRIVATION AND DEPRESSION

快速眼动睡眠剥夺和抑郁

• 批准号: 3379432
• 负责人: GERALD W VOGEL
• 金额: $ 7.86万
• 依托单位: EMORY UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1985
• 资助国家: 美国
• 起止时间: 1985-07-01 至 1989-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3379432
• 关键词: REM sleep; aggression; amitriptyline; antidepressants; behavior disorders; depression; disease /disorder model; drug administration rate /duration; drug withdrawal; eating; electrophysiology; imipramine; infant animal; mature animal; model design /development; online computer; psychopharmacology; sex behavior; sleep deprivation; sleep disorders

Isolated studies have produced empirically unconnected observations about endogenous depression and REM sleep. Our objective is to connect these observations by a web of related experiments on the same individuals. This is best done in animals. Our start is work on validity of a new animal model of endogenous depression and its treatment. Improvement of human endogenous depression by imipramine correlates with improvement in REM depriving awakenings and improvement by either correlates with posttreatment REM rebound. In animals REM depriving awakenings increase behaviors that are decreased in human endogenous depression. This suggests that animal Behavioral Activation may model a human antidepressant process. Our specific aims are tests of whether in rats, as in endogenous depressives, Behavioral Activation by either REM deprivation or imipramine will correlate with Behavioral Activation by the other treatment and with posttreatment REM rebound. In rats postnatal REM deprivation produces adults with some behavioral and REM sleep abnormalities of endogenous depression. The adult rats may model endogenous depression. Our specific aims are to test whether the adult rats will have other behavioral and REM sleep abnormalities of endogenous depression and its treatment responses (Behavioral Activation with antidepressant treatments). In rats brief REM deprivation has delayed effects. Weeks later, motor responses to antidepressant drugs are increased, suggesting that interrupted treatment may be more efficacious than continuous treatment. Our specific aim is to test the hypothesis that a second brief course of REM depriving, antidepressant treatments, weeks after a first course, will activate rat behaviors more than a first course. If successful, our animal models of endogenous depression and its treatment would have broad validity: many behavioral, REM sleep, and treatment characteristics of endogenous depression. The model could be used to study brain processes in depression and its treatment, screen new treatments, improve therapeutic efficacy, and both confirm and expand the matrix of variables concerned with endogenous depression.

孤立的研究已经产生了关于经验无关的观察结果 内源性抑郁和REM睡眠。 我们的目标是将这些联系 通过对同一个人的相关实验网的观察。 这 最好在动物中完成。 我们的开始是在新动物的有效性上工作 内源性抑郁及其治疗的模型。 人类的改善 丙咪嗪内源性抑郁症与REM的改善相关 剥夺觉醒和改进，这两种 治疗后REM反弹。 在动物中，剥夺觉醒的增加 人类内源性抑郁症的行为减少。 这暗示着 动物行为激活可能对人类抗抑郁药进行建模 过程。 我们的具体目的是测试大鼠，例如内源性 抑郁症，REM剥夺或丙咪嗪的行为激活 将与其他治疗的行为激活以及 治疗后REM反弹。 在大鼠中产后剥夺产生 具有某种行为和REM睡眠异常的成年人的内源性异常 沮丧。 成年大鼠可能会模拟内源性抑郁症。 我们的具体 目的是测试成年大鼠是否具有其他行为和REM 内源性抑郁症及其治疗反应的睡眠异常 （抗抑郁治疗的行为激活）。 在大鼠短暂的雷姆 剥夺的影响延迟。 几周后，电动机对 抗抑郁药增加了，表明治疗中断 可能比连续治疗更有效。 我们的具体目的是 检验第二个简短剥夺过程的假设， 抗抑郁药在第一疗程后数周，将激活大鼠 行为不仅仅是一门课程。 如果成功，我们的动物模型 内源性抑郁及其治疗将具有广泛的有效性：许多 行为，REM睡眠和内源性的治疗特征 沮丧。 该模型可用于研究抑郁症的大脑过程 及其治疗，筛查新治疗，提高治疗功效以及 确认并扩展了与内源性有关的变量的矩阵 沮丧。