Temporal restriction of feeding can entrain circadian behavioral and physiological rhythms in mammals. These changes in biological rhythms are postulated to be brought about by a putative food-entrainable oscillator (FEO) that is independent of the suprachiasmatic nucleus (SCN). However, the anatomical substrates and molecular machinery of FEO remain elusive. We report here that mice with a nervous system-specific deletion of Bmal1, an essential clock component, had a marked deficit in entrainment of locomotor activity by periodic feeding, accompanied by reduced food intake and subsequent loss of body weight. These mice exhibited a nearly normal light-entrainable activity rhythm driven by the SCN, because deletion of the Bmal1 gene in the SCN was only partial. These findings suggest that an SCN-independent FEO in the nervous system requires Bmal1 and plays a critical role in adaptation of circadian locomotor activity and food intake to periodic feeding.