Bidirectional interactions between the circadian and reward systems: is restricted food access a unique zeitgeber?

Authors

  • Ian C. Webb,

    1. Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada
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  • Ricardo M. Baltazar,

    1. Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada
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  • Michael N. Lehman,

    1. Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada
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  • Lique M. Coolen

    1. Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada
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Dr L. M. Coolen, as above.
E-mail: lique.coolen@schulich.uwo.ca

Abstract

Reward is mediated by a distributed series of midbrain and basal forebrain structures collectively referred to as the brain reward system. Recent evidence indicates that an additional regulatory system, the circadian system, can modulate reward-related learning. Diurnal or circadian changes in drug self-administration, responsiveness to drugs of abuse and reward to natural stimuli have been reported. These variations are associated with daily rhythms in mesolimbic electrical activity, dopamine synthesis and metabolism, and local clock gene oscillations. Conversely, the presentation of rewards appears capable of influencing circadian timing. Rodents can anticipate a daily mealtime by the entrainment of a series of oscillators that are anatomically distinct from the suprachiasmatic nucleus. Other work has indicated that restricted access to non-nutritive reinforcers (e.g. drugs of abuse, sex) or to palatable food in the absence of an energy deficit is capable of inducing relatively weak anticipatory activity, suggesting that reward alone is sufficient to induce anticipation. Recent attempts to elucidate the neural correlates of anticipation have revealed that both restricted feeding and restricted palatable food access can entrain clock gene expression in many reward-related corticolimbic structures. By contrast, restricted feeding alone can induce or entrain clock gene expression in hypothalamic nuclei involved in energy homeostasis. Thus, under ad libitum feeding conditions, the weak anticipatory activity induced by restricted reward presentation may result from the entrainment of reward-associated corticolimbic structures. The additional induction or entrainment of oscillators in hypothalamic regulatory areas may contribute to the more robust anticipatory activity associated with restricted feeding schedules.

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