REM sleep disregulation is specific for depression, and it has been suggested to constitute a vulnerability marker to relapse or reoccurrence. REM latency), enhanced REM sleep amount, prolongation of the first REM episode, reduction of slow wave sleep (SWS), disturbed sleep continuity and greater number of stage shifts (see - for review). Depressed patients often suffer from insomnia, and the polysomnographic recordings showed reduced interval between the sleep onset and the occurrence of the first rapid eye movement (REM) sleep episode (i.e. Markov analysis is a suitable method to study the sleep pattern.ĭisturbed sleep pattern might be involved in the onset and course of depression. These data might support the antidepressant activity of SSRIs, and may allude that investigating the rebound period following the flower pot protocol could be useful to detect antidepressant drug response. In conclusion, chronic SSRI treatment is capable of reducing several effects on sleep which might be the consequence of the sub-chronic stress caused by the flower pot method. Conversely, based on the aggregate sleep metrics, escitalopram had only moderate effects and it did not significantly attenuate the REM rebound after RD. The spectral analysis showed that the SSRI prevented the RD-caused elevation in theta (5-9 hz) power during slow-wave sleep. Additionally, the antidepressant avoided the frequent awakenings during the first 30 min of recovery period. The observed sleep patterns were characterized applying standard sleep metrics, by modelling the transitions between sleep phases using Markov chains and by spectral analysis.īased on Markov chain analysis, chronic escitalopram treatment attenuated the REM sleep fragmentation during the rebound sleep. On day 24, fronto-parietal electroencephalogram, electromyogram and motility were recorded in the first 2 h of the passive phase. ResultsĬhronic escitalopram- (10 mg/kg/day, osmotic minipump for 24 days) or vehicle-treated rats were subjected to a 3-day-long RD on day 21 using the flower pot procedure or kept in home cage. However, their therapeutic outcome evolves only after weeks of treatment, and the effects of chronic treatment in REM-deprived animals have not been studied yet. The selective serotonin reuptake inhibitor (SSRI) antidepressants reduce REM sleep time and increase REM latency after acute dosing in normal condition and even during REM rebound following RD. Furthermore, REM sleep fragmentation is typically associated with stress procedures and anxiety. These sleep alterations are also observable in several animal models of depression as well as during the rebound sleep after selective REM sleep deprivation (RD). Shortened rapid eye movement (REM) sleep latency and increased REM sleep amount are presumed biological markers of depression.
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