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Objective Depression in humans is associated with sleep abnormalities of three types: altered rapid eye movement (REM) sleep, fragmented sleep, and reduced delta sleep.However, the cause and effects between depression and sleep abnormalities remain debated.Methods Bilateral olfactory bulbectomy (OBX) was carried out to make a depressive model in rats.Sleep-wake profiles were assayed by the cutting-edge sleep bioassay system, and depressive behaviors were identified by open-field and forced swimming test.The contents of monoamine and their metabolites in the brain were determined by HPLC-ECD.Results (1) OBX rats exhibited a significant increase in REM sleep, especially the last 6-h during the light-on periods and attenuated non-REM sleep rebounds than sham rats after 6-h sleep deprivation (SD).(2) After acute treatment with fluoxetine (10 mg/kg, i.p.), the OBX-induced increase in REM sleep was abolished immediately, but the hyperactivity and the enhancement of immobility time remained unchanged.(3) Neurochemistry studies revealed that acute administration of fluoxetine increased the contents of serotonin (5-HT) in the hippocampus, thalamus and midbrain; decreased 5-hydroxyindoleacetic acid (5-HIAA) as well as the turnover of 5-HT (5-HIAA/5-HT) in almost all regions of the brain.Conclusion These results indicate that REM sleep abnormalities, but not the depressive behavior in OBX rats were reversed by acute administration of fluoxetine, and that there was no causality between REM abnormality and depression.