Behavioral sleep-wake homeostasis and EEG delta power are decoupled by chronic sleep restriction in the rat.

STUDY OBJECTIVES

Chronic sleep restriction (CSR) is prevalent in society and is linked to adverse consequences that might be ameliorated by acclimation of homeostatic drive. This study was designed to test the hypothesis that the sleep-wake homeostat will acclimatize to CSR.

DESIGN

A four-parameter model of proportional control was used to quantify sleep homeostasis with and without recourse to a sleep intensity function.

SETTING

Animal laboratory, rodent walking-wheel apparatus.

SUBJECTS

Male Sprague-Dawley rats.

INTERVENTIONS

Acute total sleep deprivation (TSD, 1 day × 18 or 24 h, N = 12), CSR (10 days × 18 h TSD, N = 5, or 5 days × 20 h TSD, N = 6).

MEASUREMENTS AND RESULTS

Behavioral rebounds were consistent with model predictions for proportional control of cumulative times in wake, nonrapid eye movement (NREM) and rapid eye movement (REM). Delta (D) energy homeostasis was secondary to behavioral homeostasis; a biphasic NREM D power rebound contributed to the dynamics (rapid response) but not to the magnitude of the rebound in D energy. REM behavioral homeostasis was little affected by CSR. NREM behavioral homeostasis was attenuated in proportion to cumulative NREM deficit, whereas the biphasic NREM D power rebound was only slightly suppressed, indicating decoupled regulatory mechanisms following CSR.

CONCLUSIONS

We conclude that sleep homeostasis is achieved through behavioral regulation, that the NREM behavioral homeostat is susceptible to attenuation during CSR and that the concept of sleep intensity is not essential in a model of sleep-wake regulation.

STUDY OBJECTIVES

Chronic sleep restriction (CSR) is prevalent in society and is linked to adverse consequences that might be ameliorated by acclimation of homeostatic drive. This study was designed to test the hypothesis that the sleep-wake homeostat will acclimatize to CSR.

DESIGN

A four-parameter model of proportional control was used to quantify sleep homeostasis with and without recourse to a sleep intensity function.

SETTING

Animal laboratory, rodent walking-wheel apparatus.

SUBJECTS

Male Sprague-Dawley rats.

INTERVENTIONS

Acute total sleep deprivation (TSD, 1 day × 18 or 24 h, N = 12), CSR (10 days × 18 h TSD, N = 5, or 5 days × 20 h TSD, N = 6).

MEASUREMENTS AND RESULTS

Behavioral rebounds were consistent with model predictions for proportional control of cumulative times in wake, nonrapid eye movement (NREM) and rapid eye movement (REM). Delta (D) energy homeostasis was secondary to behavioral homeostasis; a biphasic NREM D power rebound contributed to the dynamics (rapid response) but not to the magnitude of the rebound in D energy. REM behavioral homeostasis was little affected by CSR. NREM behavioral homeostasis was attenuated in proportion to cumulative NREM deficit, whereas the biphasic NREM D power rebound was only slightly suppressed, indicating decoupled regulatory mechanisms following CSR.

CONCLUSIONS

We conclude that sleep homeostasis is achieved through behavioral regulation, that the NREM behavioral homeostat is susceptible to attenuation during CSR and that the concept of sleep intensity is not essential in a model of sleep-wake regulation.