The Effects of Sleep Deprivation on the Circadian Rhythm of Plasma Cortisol Levels in Depressive Patients

Yamaguchi, Naohiko; Maeda, Kiyoshi; Kuromaru, Shoshiro

doi:10.1111/j.1440-1819.1978.tb00155.x

Cited by 23 publications

(11 citation statements)

References 30 publications

(3 reference statements)

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“…The biphasic corticosterone response induced by SD conforms to the adaptive pattern of the neuroendocrine stress response. These results are in line with several studies reporting an elevation of cortisol levels during one night of total SD (Balbo et al, 2010;Baumgartner et al, 1990;Bouhuys et al, 1990;Sgoifo et al, 2006;Voderholzer et al, 2004;von Treuer et al, 1996;Weibel et al, 1995;Weitzman et al, 1983;Yamaguchi et al, 1978). Moreover, these data also support our previous findings suggesting that a fault in the initial adaptive endogenous response of the HPA-axis unfavorably alters the trajectory of trauma exposure (Cohen et al, 2008(Cohen et al, , 2011bKozlovsky et al, 2009b;Zohar et al, 2011).…”

Section: Figuresupporting

confidence: 94%

Post-Exposure Sleep Deprivation Facilitates Correctly Timed Interactions Between Glucocorticoid and Adrenergic Systems, which Attenuate Traumatic Stress Responses

Cohen

Kozlovsky

Matar

et al. 2012

Neuropsychopharmacol

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Reliable evidence supports the role of sleep in learning and memory processes. In rodents, sleep deprivation (SD) negatively affects consolidation of hippocampus-dependent memories. As memory is integral to post-traumatic stress symptoms, the effects of postexposure SD on various aspect of the response to stress in a controlled, prospective animal model of post-traumatic stress disorder (PTSD) were evaluated. Rats were deprived of sleep for 6 h throughout the first resting phase after predator scent stress exposure. Behaviors in the elevated plus-maze and acoustic startle response tests were assessed 7 days later, and served for classification into behavioral response groups. Freezing response to a trauma reminder was assessed on day 8. Urine samples were collected daily for corticosterone levels, and heart rate (HR) was also measured. Finally, the impact of manipulating the hypothalamus-pituitary-adrenal axis and adrenergic activity before SD was assessed. Mifepristone (MIFE) and epinephrine (EPI) were administered systemically 10-min poststress exposure and behavioral responses and response to trauma reminder were measured on days 7-8. Hippocampal expression of glucocorticoid receptors (GRs) and morphological assessment of arborization and dendritic spines were subsequently evaluated. Postexposure SD effectively ameliorated long-term, stress-induced, PTSD-like behavioral disruptions, reduced trauma reminder freezing responses, and decreased hippocampal expression of GR compared with exposed-untreated controls. Although urine corticosterone levels were significantly elevated 1 h after SD and the HR was attenuated, antagonizing GRs with MIFE or stimulation of adrenergic activity with EPI effectively abolished the effect of SD. MIFE-and EPI-treated animals clearly demonstrated significantly lower total dendritic length, fewer branches and lower spine density along dentate gyrus dendrites with increased levels of GR expression 8 days after exposure, as compared with exposed-SD animals. Intentional prevention of sleep in the early aftermath of stress exposure may well be beneficial in attenuating traumatic stress-related sequelae. Post-exposure SD may disrupt the consolidation of aversive or fearful memories by facilitating correctly timed interactions between glucocorticoid and adrenergic systems.

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Section: Figuresupporting

confidence: 94%

Post-Exposure Sleep Deprivation Facilitates Correctly Timed Interactions Between Glucocorticoid and Adrenergic Systems, which Attenuate Traumatic Stress Responses

Cohen

Kozlovsky

Matar

et al. 2012

Neuropsychopharmacol

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“…In depressives the mean values of cortisol on the day following SD are higher compared to those on the preceding day. In the patients responding well to SD, the variation of cortisol mean values which was obscure the preceding day showed an evident rhythm the following day (Yamaguchi et al 1978). Free urinary cortisol is found in larger quantities in depressives than in healthy controls and the amount of cortisol is again raised after a period of SD with a and simultaneous increase in amplitude (Goetze & Tolle, 1987).…”

Section: Discussionmentioning

confidence: 90%

White blood cells and cortisol after sleep deprivation and recovery sleep in humans

Heiser¹,

Dickhaus

Schreiber

et al. 2000

European Archives of Psychiatry and Clinical Neurosciences

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Sleep deprivation (SD) has enriched our treatment programme for major depression. SD has been demonstrated to modify different host defence activities. There is some evidence that there are reciprocal relationships between immune function and increased hypothalamic-pituitary-adrenocortical (HPA) axis activity in depression. We therefore investigated the number of leukocytes, granulocytes, monocytes, lymphocytes, B cells, T cells, helper T cells, cytotoxic T cells, NK cells and salivary cortisol in 10 healthy men before and after total SD (TSD) as well as after recovery sleep. Blood samples were drawn on 3 consecutive days at 7 am, 1 pm and 7 pm, respectively. Comparison of the 7 am values by contrast analysis yielded significant differences for granulocytes (p = 0.044) and NK cells (p = 0.001) after SD and recovery sleep. NK cells decreased and granulocytes increased after SD and after recovery sleep. Significant differences between single points in time across the day were found for granulocytes (p = 0.022), monocytes (p = 0.031), T cells (p = 0.005), helper T cells (p = 0.004), cytotoxic T cells (p = 0.005) and NK cells (p = 0.017). No significant difference could be detected for leukocytes, lymphocytes and B cells counts. These results favour the thesis that SD and recovery sleep lead to changes in the distribution of peripheral leukocytes, especially in a reduction of NK cells after SD and recovery sleep. The cortisol rhythm was affected neither by SD nor recovery sleep.

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“…It therefore en sues that sleep deprivation counteracts or constrains the sleep-induced restraints of cortisol excretion. Yamaguchi et al [1978] emphasize the different effects of sleep deprivation on cortisol production in depressives in comparison with healthy subjects.…”

Section: Discussionmentioning

confidence: 99%

Circadian Rhythm of Free Urinary Cortisol, Temperature and Heart Rate in Endogenous Depressives and under Antidepressant Therapy

Goetze¹,

Tölle²

1987

Neuropsychobiology

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Free cortisol in urine, temperature and heart rate were examined in 81 endogenous depressives and 15 healthy controls in five successive 24-hour rhythms. The nocturnal mean value, amplitude, phase position of the minima and period length were calculated. Main results: cortisol secretion is to be found in larger quantities in depressives than in healthy controls. The amount of cortisol is again raised after a period of sleep deprivation and simultaneously the amplitude becomes larger. Temperature measurements revealed an enlargement of the amplitude following treatment with tricyclic antidepressants. A minimal increase in heart rate is evident in endogenous depressives in comparison with healthy subjects. The heart rate in the entire circadian course is significantly increased by antidepressants. All three variables showed a phase advance of the nocturnal minima in endogenous depression. Alterations in period length could not be detected. The findings were discussed in regard to chronobiological dissertations on endogenous depression.

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The Effects of Sleep Deprivation on the Circadian Rhythm of Plasma Cortisol Levels in Depressive Patients

Cited by 23 publications

References 30 publications

Post-Exposure Sleep Deprivation Facilitates Correctly Timed Interactions Between Glucocorticoid and Adrenergic Systems, which Attenuate Traumatic Stress Responses

Post-Exposure Sleep Deprivation Facilitates Correctly Timed Interactions Between Glucocorticoid and Adrenergic Systems, which Attenuate Traumatic Stress Responses

White blood cells and cortisol after sleep deprivation and recovery sleep in humans

Circadian Rhythm of Free Urinary Cortisol, Temperature and Heart Rate in Endogenous Depressives and under Antidepressant Therapy

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