In nocturnal rodents, restricted feeding to daytime (RF) causes feeding-associated diurnal locomotor activity that persists for the next 1-2 days when food is withheld. Along with this anticipatory behavior, the expression pattern of clock genes such as mPer1 and mPer2 changes from a nocturnal to diurnal pattern in the liver and cerebral cortex but not in the suprachiasmatic nucleus (SCN). Whether the molecular clockwork, in which mCry1 and mCry2 genes are essential components, is involved in food-anticipatory circadian rhythms is unknown. In this study, we investigated the impact of the absence of mCRY products upon the locomotion pattern induced by RF. RF caused an increase in daytime activity that lasted even for 2 days after food was withheld, in wild-type and mCry1-/- mCry2-/- mice. However, RF-induced activity was less stable and appeared more gradually in mutant mice. Similar results were obtained with mice housed under constant darkness or with SCN-lesioned wild-type and mutant mice. Our data reveal that mCry proteins are basically dispensable for food-entrainable oscillation. However, it is also important to note that mCry deficiency affects the stability and development of RF-induced anticipatory locomotor activity.
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