Unlimited sucrose consumption during adolescence generates a depressive-like phenotype in adulthood

Aliou B. Gueye, Leandro F. Vendruscolo, Camila de Ávila, Catherine Le Moine, Muriel Darnaudéry, Martine Cador
Neuropsychopharmacol. 2018-12-27; 43(13): 2627-2635
DOI: 10.1038/s41386-018-0025-9

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Gueye AB(1)(2)(3), Vendruscolo LF(1)(2)(4), de Ávila C(5)(6)(7), Le Moine C(1)(2), Darnaudéry M(5)(6), Cador M(8)(9).

Author information:
(1)Université Bordeaux, INCIA, UMR 5287, Bordeaux, F-33000, France.
(2)CNRS, INCIA, UMR 5287, Bordeaux, F-33000, France.
(3)Département de pharmacologie et physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada.
(4)Neurobiology of Addiction Section, NIDA-IRP, NIH, Baltimore, Md, USA.
(5)INRA, Lab. Nutrition et Neurobiologie Intégrée, UMR1286, Bordeaux, France.
(6)Lab. Nutrition et Neurobiologie Intégrée, UMR1286, Université de Bordeaux, Bordeaux, France.
(7)Faculté de Médecine, Département de Psychiatrie et de Neurosciences, Centre de recherche de l’Institut universitaire de cardiologie et de pneumologie de Québec, Université Laval, Québec, QC, G1V 0A6, Canada.
(8)Université Bordeaux, INCIA, UMR 5287, Bordeaux, F-33000, France. .
(9)CNRS, INCIA, UMR 5287, Bordeaux, F-33000, France. .

Depression is highly prevalent worldwide, but its etiology is not fully understood. An overlooked possible contributor to the epidemic of depression is feeding styles, particularly at early age when the brain is intensely changing. We have previously reported that unlimited sucrose consumption during adolescence
leads to enduring changes in brain reward function. Here, we tested the hypothesis that sucrose consumption during adolescence would lead to a ‘depressive-like’ phenotype. Adolescent male rats were given unlimited access to 5% sucrose in their home cages from postnatal day 30 to postnatal day 46 and their emotional behavior was subsequently examined at adulthood. Sucrose consumption during adolescence caused anhedonia, decreased motivation for saccharin, increased immobility in the forced swim test and exacerbated
anxiety-like behavior. Additionally, sucrose consumption during adolescence decreased cell proliferation in the hippocampus in adulthood. Chronic treatment with imipramine (10 mg/kg) normalized behavior and restored cell proliferation in the hippocampus of adult rats with a history of sucrose consumption during adolescence. A similar sucrose consumption starting at adulthood only increases immobility in the forced swim test, suggesting that sucrose intake affects also adults’ behavior but to a lesser degree. Overall, our findings reveal an unsuspected protracted effect of sucrose consumption on behavior and suggest that unlimited sucrose consumption during critical periods of brain development may play an important role in the etiology of reward-related disorders such as depression.

Auteurs Bordeaux Neurocampus