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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

Theta/Delta. Theta/delta ratio is shown as mean of the total power in fast the θ (6.6–9.0 Hz) band divided by total power in fast δ (2.5–4.0 Hz) band, computed throughout ~11 hours period in the light and dark phases of the recovery period. ACSF, artificial cerebrospinal fluid; CRH, corticotrophin-releasing hormone; αhCRH, alpha helical CRH9−41; AW, active wake; QW, quiet wake; L NREM, low amplitude NREM sleep; H NREM, high amplitude NREM sleep; PS, REM sleep; Rec. Recovery period. The white panels indicate the light phase and the gray ones, the dark phase. *- different from baseline, #-different from ACSF group, and ‡- different from αhCRH group. Main effects of sleep parameter are indicated by connecting lines above the bars. ANCOVA, followed by the Newman-Keuls test, P ≤ .05.
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fig6: Theta/Delta. Theta/delta ratio is shown as mean of the total power in fast the θ (6.6–9.0 Hz) band divided by total power in fast δ (2.5–4.0 Hz) band, computed throughout ~11 hours period in the light and dark phases of the recovery period. ACSF, artificial cerebrospinal fluid; CRH, corticotrophin-releasing hormone; αhCRH, alpha helical CRH9−41; AW, active wake; QW, quiet wake; L NREM, low amplitude NREM sleep; H NREM, high amplitude NREM sleep; PS, REM sleep; Rec. Recovery period. The white panels indicate the light phase and the gray ones, the dark phase. *- different from baseline, #-different from ACSF group, and ‡- different from αhCRH group. Main effects of sleep parameter are indicated by connecting lines above the bars. ANCOVA, followed by the Newman-Keuls test, P ≤ .05.

Mentions: On the second recovery day, αhCRH led to increased power in the 1.0–3.0 Hz bands (average of 4 bins of 0.5 Hz each = 53.7%, P ≤ .05), when compared to ACSF group and increased all bands above 6.0 Hz when compared to CRH-treated rats (average of 19 bins of 1.0 Hz each = 28.5%, P ≤ .05). Finally, during the last recovery day, αhCRH produced an increase in all bands above 7.0 Hz when compared to CRH-treated animals (average of 18 bins of 1.0 Hz each = 27.1%, 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)

Theta/Delta. Theta/delta ratio is shown as mean of the total power in fast the θ (6.6–9.0 Hz) band divided by total power in fast δ (2.5–4.0 Hz) band, computed throughout ~11 hours period in the light and dark phases of the recovery period. ACSF, artificial cerebrospinal fluid; CRH, corticotrophin-releasing hormone; αhCRH, alpha helical CRH9−41; AW, active wake; QW, quiet wake; L NREM, low amplitude NREM sleep; H NREM, high amplitude NREM sleep; PS, REM sleep; Rec. Recovery period. The white panels indicate the light phase and the gray ones, the dark phase. *- different from baseline, #-different from ACSF group, and ‡- different from αhCRH group. Main effects of sleep parameter are indicated by connecting lines above the bars. ANCOVA, followed by the Newman-Keuls test, P ≤ .05.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig6: Theta/Delta. Theta/delta ratio is shown as mean of the total power in fast the θ (6.6–9.0 Hz) band divided by total power in fast δ (2.5–4.0 Hz) band, computed throughout ~11 hours period in the light and dark phases of the recovery period. ACSF, artificial cerebrospinal fluid; CRH, corticotrophin-releasing hormone; αhCRH, alpha helical CRH9−41; AW, active wake; QW, quiet wake; L NREM, low amplitude NREM sleep; H NREM, high amplitude NREM sleep; PS, REM sleep; Rec. Recovery period. The white panels indicate the light phase and the gray ones, the dark phase. *- different from baseline, #-different from ACSF group, and ‡- different from αhCRH group. Main effects of sleep parameter are indicated by connecting lines above the bars. ANCOVA, followed by the Newman-Keuls test, P ≤ .05.
Mentions: On the second recovery day, αhCRH led to increased power in the 1.0–3.0 Hz bands (average of 4 bins of 0.5 Hz each = 53.7%, P ≤ .05), when compared to ACSF group and increased all bands above 6.0 Hz when compared to CRH-treated rats (average of 19 bins of 1.0 Hz each = 28.5%, P ≤ .05). Finally, during the last recovery day, αhCRH produced an increase in all bands above 7.0 Hz when compared to CRH-treated animals (average of 18 bins of 1.0 Hz each = 27.1%, 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