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

Machado RB, Tufik S, Suchecki D - Int J Endocrinol (2010)

Bottom Line: Throughout 96 hours of sleep deprivation, separate groups of rats were treated i.c.v. with vehicle, CRH or with alphahelical CRH(9-41), a CRH receptor blocker, twice/day, at 07:00 h and 19:00 h.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.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Psicobiologia, Universidade Federal de São Paulo, 04024-002 São Paulo, Brazil.

ABSTRACT
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 CRH(9-41), 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.

No MeSH data available.


Related in: MedlinePlus

ACTH and CORT Plasma Levels. CTL, Control; ACSF, artificial cerebrospinal fluid; CRH, corticotrophin-releasing hormone; αhCRH, alpha-helical CRH9−41*- different from CTL+ACSF, #- different from PSD+ACSF, and †- different from CTL+CRH, ‡- different from CTL+αhCRH; ANOVA, followed by Newman-Keuls test, P ≤ .05.
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fig1: ACTH and CORT Plasma Levels. CTL, Control; ACSF, artificial cerebrospinal fluid; CRH, corticotrophin-releasing hormone; αhCRH, alpha-helical CRH9−41*- different from CTL+ACSF, #- different from PSD+ACSF, and †- different from CTL+CRH, ‡- different from CTL+αhCRH; ANOVA, followed by Newman-Keuls test, P ≤ .05.

Mentions: Hormonal data were analyzed by a two-way ANOVA, with main factor Group (CTL—control home cage and REM sleep deprivation—REMSD) and Treatment (ACSF, CRH, and αhCRH). Sleep parameters were analyzed by a two-way ANOVA for repeated measures, with main factors Treatment (ACSF, CRH, and αhCRH) and Day (repeated measure: Baseline and Recovery days 1 [R1], 2 [R2], and 3 [R3]). The spectra power density was analyzed by Student's t tests for independent samples, every 12 hours period, for each behavioral state separately. The theta-delta ratio was analyzed by covariance analyses (ANCOVA) where the baseline index was the predictive factor and treatments, the independent variable. All EEG data were analyzed during the light and dark phases, separately. Posthoc analysis was performed by the Newman-Keuls test. The level of significance was set at P ≤ .05.


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

Machado RB, Tufik S, Suchecki D - Int J Endocrinol (2010)

ACTH and CORT Plasma Levels. CTL, Control; ACSF, artificial cerebrospinal fluid; CRH, corticotrophin-releasing hormone; αhCRH, alpha-helical CRH9−41*- different from CTL+ACSF, #- different from PSD+ACSF, and †- different from CTL+CRH, ‡- different from CTL+αhCRH; ANOVA, followed by Newman-Keuls test, P ≤ .05.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2902042&req=5

fig1: ACTH and CORT Plasma Levels. CTL, Control; ACSF, artificial cerebrospinal fluid; CRH, corticotrophin-releasing hormone; αhCRH, alpha-helical CRH9−41*- different from CTL+ACSF, #- different from PSD+ACSF, and †- different from CTL+CRH, ‡- different from CTL+αhCRH; ANOVA, followed by Newman-Keuls test, P ≤ .05.
Mentions: Hormonal data were analyzed by a two-way ANOVA, with main factor Group (CTL—control home cage and REM sleep deprivation—REMSD) and Treatment (ACSF, CRH, and αhCRH). Sleep parameters were analyzed by a two-way ANOVA for repeated measures, with main factors Treatment (ACSF, CRH, and αhCRH) and Day (repeated measure: Baseline and Recovery days 1 [R1], 2 [R2], and 3 [R3]). The spectra power density was analyzed by Student's t tests for independent samples, every 12 hours period, for each behavioral state separately. The theta-delta ratio was analyzed by covariance analyses (ANCOVA) where the baseline index was the predictive factor and treatments, the independent variable. All EEG data were analyzed during the light and dark phases, separately. Posthoc analysis was performed by the Newman-Keuls test. The level of significance was set at P ≤ .05.

Bottom Line: Throughout 96 hours of sleep deprivation, separate groups of rats were treated i.c.v. with vehicle, CRH or with alphahelical CRH(9-41), a CRH receptor blocker, twice/day, at 07:00 h and 19:00 h.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.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Psicobiologia, Universidade Federal de São Paulo, 04024-002 São Paulo, Brazil.

ABSTRACT
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 CRH(9-41), 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.

No MeSH data available.


Related in: MedlinePlus