Long-lasting deficits in hedonic and nucleus accumbens reactivity to sweet rewards by sugar overconsumption during adolescence
Eur J Neurosci. 2016-01-13; 43(5): 671-680
DOI: 10.1111/ejn.13149
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Naneix F(1)(2), Darlot F(1)(2), Coutureau E(1)(2), Cador M(1)(2).
Author information:
(1)CNRS, Institut de Neurosciences Cognitives et Intégratives d’Aquitaine, UMR 5287, Bordeaux, France.
(2)University of Bordeaux, Institut de Neurosciences Cognitives et Intégratives d’Aquitaine, UMR 5287, F-33076, Bordeaux, France.
Adolescence is a critical period characterized by major neurobiological changes.
Chronic stimulation of the reward system might constitute an important factor in
vulnerability to pathological development. In spite of the dramatic increase in
the consumption of sweet palatable foods during adolescence in our modern
societies, the long-term consequences of such exposure on brain reward processing
remain poorly understood. Here, we investigated in rats the long-lasting effects
of sugar overconsumption during their adolescence on their adult reactivity to
the hedonic properties of sweet rewards. Adolescent rats with continuous access
to 5% sucrose solution (from postnatal day 30-46) showed escalating intake. At
adulthood (post-natal day 70), using two-bottle free choice tests,
sucrose-exposed rats showed lower intake than non-exposed rats suggesting
decreased sensitivity to the rewarding properties of sucrose. In Experiment 1, we
tested their hedonic-related orofacial reactions to intraoral infusion of tasty
solutions. We showed that sucrose-exposed rats presented less hedonic reactions
in response to sweet tastes leaving the reactivity to water or quinine unaltered.
Hence, in Experiment 2, we observed that this hedonic deficit is associated with
lower c-Fos expression levels in the nucleus accumbens, a brain region known to
play a central role in hedonic processing. These findings demonstrate that a
history of high sucrose intake during the critical period of adolescence induces
long-lasting deficits in hedonic treatment that may contribute to reward-related
disorders.
© 2016 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.