Nutritional omega-3 modulates neuronal morphology in the prefrontal cortex along with depression-related behaviour through corticosterone secretion.

T Larrieu, L M Hilal, C Fourrier, V De Smedt-Peyrusse, Sans N, L Capuron, S Layé
Transl Psychiatry. 2014-09-01; 4(9): e437-e437
DOI: 10.1038/tp.2014.77

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Larrieu T(1), Hilal ML, Fourrier C(1), De Smedt-Peyrusse V(1), Sans N(2), Capuron L(1), Layé S(1).

Author information:
(1)1] INRA, Nutrition et Neurobiologie Intégrée, UMR 1286, Bordeaux, France [2] Universite de Bordeaux, Nutrition et Neurobiologie intégrée, UMR 1286, Bordeaux, France.
(2)1] INSERM, Neurocentre Magendie, UMR 862, Bordeaux, France [2] Universite de Bordeaux, Neurocentre Magendie, UMR 862, Bordeaux, France.

Erratum in
Transl Psychiatry. 2014;4:e468. Hilal, L M [corrected to Hilal, M L]; N, Sans [corrected to Sans, N].

Understanding how malnutrition contributes to depression is building momentum. In the present study we unravel molecular and cellular mechanisms by which nutritional disturbances lead to impaired emotional behaviour in mice. Here we report that nutritional n-3 polyunsaturated fatty acids (PUFA) deficiency induces a chronic stress state reflected by disrupted glucocorticoid receptor (GR)-mediated signalling pathway along with hypothalamic-pituitary-adrenal (HPA) axis hyperactivity. This hyperactivity in turn resulted in neuronal atrophy in the dorsolateral (dl)- and dorsomedial (dm)- prefrontal cortex (PFC) and subsequent mood-related behaviour alterations, similarly to chronic social defeat stress. Supplementation of n-3 PUFA prevented detrimental chronic social defeat stress-induced emotional and neuronal impairments by impeding HPA axis hyperactivity. These results indicate a role for dietary n-3 PUFA in the prevention of HPA axis dysfunction associated with the development of some neuropsychiatric disorders including depression.


Auteurs Bordeaux Neurocampus