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 i s 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.
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