Chronobiology internationalAug 30, 2012

Scheduled feeding changes the daily clock timing in the brain's main circadian center of mice lacking Dexras1

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Updated Mar 29, 2026

Abstract

Daytime restricted feeding led to a potentiated but less stable food anticipatory activity in dexras1-deficient mice compared to wild-type controls.

Restricted feeding affects metabolic and hormonal rhythms, manifesting as food anticipatory activity.
Dexras1 deficiency disrupts the stability of circadian rhythms in response to restricted feeding.
The phase and magnitude of activity regulated by the central circadian pacemaker are significantly altered in dexras1(-/-) mice.
Restoration to ad libitum feeding results in a stable phase shift of approximately 2 hours in dexras1-deficient mice.
Daytime restricted feeding influences the expression rhythms of certain genes in the SCN of dexras1-deficient mice, unlike in wild-type mice.

Simplified

Restricted feeding (RF) schedules are potent zeitgebers capable of entraining metabolic and hormonal rhythms in peripheral oscillators in anticipation of food. Behaviorally, this manifests in the form of food anticipatory activity (FAA) in the hours preceding food availability. Circadian rhythms of FAA are thought to be controlled by a food-entrainable oscillator (FEO) outside of the suprachiasmatic nucleus (SCN), the central circadian pacemaker in mammals. Although evidence suggests that the FEO and the SCN are capable of interacting functionally under RF conditions, the genetic basis of these interactions remains to be defined. In this study, using dexras1-deficient (dexras1(-/-)) mice, the authors examined whether Dexras1, a modulator of multiple inputs to the SCN, plays a role in regulating the effects of RF on activity rhythms and gene expression in the SCN. Daytime RF under 12L:12D or constant darkness (DD) resulted in potentiated (but less stable) FAA expression in dexras1(-/-) mice compared with wild-type (WT) controls. Under these conditions, the magnitude and phase of the SCN-driven activity component were greatly perturbed in the mutants. Restoration to ad libitum (AL) feeding revealed a stable phase displacement of the SCN-driven activity component of dexras1(-/-) mice by ~2 h in advance of the expected time. RF in the late night/early morning induced a long-lasting increase in the period of the SCN-driven activity component in the mutants but not the WT. At the molecular level, daytime RF advanced the rhythm of PER1, PER2, and pERK expression in the mutant SCN without having any effect in the WT. Collectively, these results indicate that the absence of Dexras1 sensitizes the SCN to perturbations resulting from restricted feeding.

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Scheduled feeding changes the daily clock timing in the brain's main circadian center of mice lacking Dexras1

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