Neuroendocrine and Peptidergic Regulation of Stress-Induced REM Sleep Rebound

Sleep homeostasis depends on the length and quality (occurrence of stressful events, for instance) of the preceding waking time. Forced wakefulness (sleep deprivation or sleep restriction) is one of the main tools used for the understanding of mechanisms that play a role in homeostatic processes involved in sleep regulation and their interrelations. Interestingly, forced wakefulness for periods longer than 24 h activates stress response systems, whereas stressful events impact on sleep pattern. Hypothalamic peptides (corticotropin-releasing hormone, prolactin, and the CLIP/ACTH (18-39)) play an important role in the expression of stress-induced sleep effects, essentially by modulating rapid eye movement sleep, which has been claimed to affect the organism resilience to the deleterious effects of stress. Some of the mechanisms involved in the generation and regulation of sleep and the main peptides/hypothalamic hormones involved in these responses will be discussed in this review.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)/Centros de Pesquisa, Inovação e Difusão (CEPID)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Univ Ibirapuera, Psychosomat Res Grp, Dept Psychol, Sao Paulo, BrazilUniv Ibirapuera, Psychosomat Res Grp, Dept Pharm, Sao Paulo, BrazilUniv Fed Sao Paulo, Escola Paulista Med, Dept Psychobiol, Sao Paulo, BrazilDepartment of Psychobiology, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, BrazilFAPESP/CEPID: 98/14303-3CNPq: 486769/2013-5FAPESP: 2010/09087-3CNPq: 302294/2012-0FAPESP: 2015/26364-4Web of Scienc

Modulation of Sleep Homeostasis by Corticotropin Releasing Hormone in REM Sleep-Deprived Rats

Studies have shown that sleep recovery following different protocols of forced waking varies according to the level of stress inherent to each method. Sleep deprivation activates the hypothalamic-pituitary-adrenal axis and increased corticotropin-releasing hormone (CRH) impairs sleep. The purpose of the present study was to evaluate how manipulations of the CRH system during the sleep deprivation period interferes with subsequent sleep rebound. Throughout 96 hours of sleep deprivation, separate groups of rats were treated i.c.v. with vehicle, CRH or with alphahelical CRH9−41, a CRH receptor blocker, twice/day, at 07:00 h and 19:00 h. Both treatments impaired sleep homeostasis, especially in regards to length of rapid eye movement sleep (REM) and theta/delta ratio and induced a later decrease in NREM and REM sleep and increased waking bouts. These changes suggest that activation of the CRH system impact negatively on the homeostatic sleep response to prolonged forced waking. These results indicate that indeed, activation of the HPA axis—at least at the hypothalamic level—is capable to reduce the sleep rebound induced by sleep deprivation

REM Sleep Rebound as an Adaptive Response to Stressful Situations

Stress and sleep are related to each other in a bidirectional way. If on one hand poor or inadequate sleep exacerbates emotional, behavioral, and stress-related responses, on the other hand acute stress induces sleep rebound, most likely as a way to cope with the adverse stimuli. Chronic, as opposed to acute, stress impairs sleep and has been claimed to be one of the triggering factors of emotional-related sleep disorders, such as insomnia, depressive- and anxiety-disorders. These outcomes are dependent on individual psychobiological characteristics, conferring even more complexity to the stress-sleep relationship. Its neurobiology has only recently begun to be explored, through animal models, which are also valuable for the development of potential therapeutic agents and preventive actions. This review seeks to present data on the effects of stress on sleep and the different approaches used to study this relationship as well as possible neurobiological underpinnings and mechanisms involved. The results of numerous studies in humans and animals indicate that increased sleep, especially the rapid eye movement phase, following a stressful situation is an important adaptive behavior for recovery. However, this endogenous advantage appears to be impaired in human beings and rodent strains that exhibit high levels of anxiety and anxiety-like behavior

Effect of fish oil and coconut fat supplementation on depressive-type behavior and corticosterone levels of prenatally stressed male rats

Prenatal stress (PNS) during critical periods of brain development has been associated with numerous behavioral and/or mood disorders in later life. These outcomes may result from changes in the hypothalamic-pituitary-adrenal (HPA) axis activity, which, in turn, can be modulated by environmental factors, such as nutritional status. in this study, the adult male offspring of dams exposed to restraint stress during the last semester of pregnancy and fed different diets were evaluated for depressive-like behavior in the forced swimming test and for the corticosterone response to the test. Female Wistar rats were allocated to one of three groups: regular diet, diet supplemented with coconut fat or with fish oil, offered during pregnancy and lactation. When pregnancy was confirmed, they were distributed into control or stress groups. Stress consisted of restraint and bright light for 45 min, three times per day, in the last week of pregnancy. the body weight of the adult offspring submitted to PNS was lower than that of controls. in the forced swimming test, time of immobility was reduced and swimming was increased in PNS rats fed fish oil and plasma corticosterone levels immediately after the forced swimming test were lower in PNS rats fed regular diet than their control counterparts; this response was reduced in control rats whose mothers were fed fish oil and coconut fat. the present results indicate that coconut fat and fish oil influenced behavioral and hormonal responses to the forced swimming test in both control and PNS adult male rats. (C) 2011 Elsevier B.V. All rights reserved.Associacao Fundo de Incentivo a Psicofarmacologia (AFIP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Universidade Federal de São Paulo, Dept Psychobiol, BR-04024002 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Psychobiol, BR-04024002 São Paulo, BrazilWeb of Scienc

Role of Corticosterone on Sleep Homeostasis Induced by REM Sleep Deprivation in Rats

Sleep is regulated by humoral and homeostatic processes. If on one hand chronic elevation of stress hormones impair sleep, on the other hand, rapid eye movement (REM) sleep deprivation induces elevation of glucocorticoids and time of REM sleep during the recovery period. in the present study we sought to examine whether manipulations of corticosterone levels during REM sleep deprivation would alter the subsequent sleep rebound. Adult male Wistar rats were fit with electrodes for sleep monitoring and submitted to four days of REM sleep deprivation under repeated corticosterone or metyrapone (an inhibitor of corticosterone synthesis) administration. Sleep parameters were continuously recorded throughout the sleep deprivation period and during 3 days of sleep recovery. Plasma levels of adrenocorticotropic hormone and corticosterone were also evaluated. Metyrapone treatment prevented the elevation of corticosterone plasma levels induced by REM sleep deprivation, whereas corticosterone administration to REM sleep-deprived rats resulted in lower corticosterone levels than in non-sleep deprived rats. Nonetheless, both corticosterone and metyrapone administration led to several alterations on sleep homeostasis, including reductions in the amount of non-REM and REM sleep during the recovery period, although corticosterone increased delta activity (1.0-4.0 Hz) during REM sleep deprivation. Metyrapone treatment of REM sleep-deprived rats reduced the number of REM sleep episodes. in conclusion, reduction of corticosterone levels during REM sleep deprivation resulted in impairment of sleep rebound, suggesting that physiological elevation of corticosterone levels resulting from REM sleep deprivation is necessary for plentiful recovery of sleep after this stressful event.Associacao Fundo de Incentivo a Pesquisa (AFIP)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Universidade Federal de São Paulo, Dept Psychobiol, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Psychobiol, São Paulo, BrazilFAPESP: 98/14303-3FAPESP: 04/02213-2Web of Scienc

Role of Corticosterone on Sleep Homeostasis Induced by REM Sleep Deprivation in Rats

Sleep is regulated by humoral and homeostatic processes. If on one hand chronic elevation of stress hormones impair sleep, on the other hand, rapid eye movement (REM) sleep deprivation induces elevation of glucocorticoids and time of REM sleep during the recovery period. in the present study we sought to examine whether manipulations of corticosterone levels during REM sleep deprivation would alter the subsequent sleep rebound. Adult male Wistar rats were fit with electrodes for sleep monitoring and submitted to four days of REM sleep deprivation under repeated corticosterone or metyrapone (an inhibitor of corticosterone synthesis) administration. Sleep parameters were continuously recorded throughout the sleep deprivation period and during 3 days of sleep recovery. Plasma levels of adrenocorticotropic hormone and corticosterone were also evaluated. Metyrapone treatment prevented the elevation of corticosterone plasma levels induced by REM sleep deprivation, whereas corticosterone administration to REM sleep-deprived rats resulted in lower corticosterone levels than in non-sleep deprived rats. Nonetheless, both corticosterone and metyrapone administration led to several alterations on sleep homeostasis, including reductions in the amount of non-REM and REM sleep during the recovery period, although corticosterone increased delta activity (1.0-4.0 Hz) during REM sleep deprivation. Metyrapone treatment of REM sleep-deprived rats reduced the number of REM sleep episodes. in conclusion, reduction of corticosterone levels during REM sleep deprivation resulted in impairment of sleep rebound, suggesting that physiological elevation of corticosterone levels resulting from REM sleep deprivation is necessary for plentiful recovery of sleep after this stressful event.Associacao Fundo de Incentivo a Pesquisa (AFIP)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Universidade Federal de São Paulo, Dept Psychobiol, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Psychobiol, São Paulo, BrazilFAPESP: 98/14303-3FAPESP: 04/02213-2Web of Scienc

Sleep and the Endocrine Brain

Univ Maryland, Dept Pharmacol & Expt Therapeut, Sch Med, Baltimore, MD 21201 USAUniv Maryland, Sch Med, Program Neurosci, Baltimore, MD 21201 USAUniversidade Federal de São Paulo, Dept Psychobiol, BR-04024002 São Paulo, BrazilDalhousie Univ, Dept Anat & Neurobiol, Halifax, NS B3H 4R2, CanadaUniv Calif San Diego, Dept Psychiat, San Diego, CA 92037 USAUniversidade Federal de São Paulo, Dept Psychobiol, BR-04024002 São Paulo, BrazilWeb of Scienc

Improvement of mood and sleep alterations in posttraumatic stress disorder patients by eye movement desensitization and reprocessing

Posttraumatic stress disorder (PTSD) patients exhibit depressive and anxiety symptoms, in addition to nightmares, which interfere with sleep continuity. Pharmacologic treatment of these sleep problems improves PTSD symptoms, but very few studies have used psychotherapeutic interventions to treat PTSD and examined their effects on sleep quality. Therefore, in the present study, we sought to investigate the effects of Eye Movement Desensitization Reprocessing therapy on indices of mood, anxiety, subjective, and objective sleep. the sample was composed of 11 healthy controls and 13 PTSD patients that were victims of assault and/or kidnapping. All participants were assessed before, and 1 day after, the end of treatment for depressive and anxiety profile, general well-being and subjective sleep by filling out specific questionnaires. in addition, objective sleep patterns were evaluated by polysomnographic recording. Healthy volunteers were submitted to the therapy for three weekly sessions, whereas PTSD patients underwent five sessions, on average. Before treatment, PTSD patients exhibited high levels of anxiety and depression, poor quality of life and poor sleep, assessed both subjectively and objectively; the latter was reflected by increased time of waking after sleep onset. After completion of treatment, patients exhibited improvement in depression and anxiety symptoms, and in quality of life; with indices that were no longer different from control volunteers. Moreover, these patients showed more consolidated sleep, with reduction of time spent awake after sleep onset. in conclusion, Eye Movement Desensitization and Reprocessing was an effective treatment of PTSD patients and improved the associated sleep and psychological symptoms.Associação Fundo de Incentivo a PesquisaFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Universidade Federal de São Paulo, Dept Psicobiol, Grp Studies Neurobiol Stress & Stress Related Dis, São Paulo, BrazilAssoc Fundo Incent Pesquisa, Inst Sono, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Psicobiol, Sleep Div, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Psicobiol, Grp Studies Neurobiol Stress & Stress Related Dis, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Psicobiol, Sleep Div, São Paulo, BrazilFAPESP: 98/14303-3Web of Scienc