Maternal high-fat diet and early life stress differentially modulate spine density and dendritic morphology in the medial prefrontal cortex of juvenile and adult rats.
Brain Struct Funct. 2017-10-11; 223(2): 883-895
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1. Brain Struct Funct. 2018 Mar;223(2):883-895. doi: 10.1007/s00429-017-1526-8. Epub
2017 Oct 11.
Maternal high-fat diet and early life stress differentially modulate spine
density and dendritic morphology in the medial prefrontal cortex of juvenile and
Rincel M(1)(2), Lépinay AL(1)(2), Janthakhin Y(1)(2), Soudain G(1)(2), Yvon S(3),
Da Silva S(3), Joffre C(1)(2), Aubert A(1)(2), Séré A(1)(2), Layé S(1)(2),
Theodorou V(3), Ferreira G(1)(2), Darnaudéry M(4)(5).
(1)UMR1286, INRA, Nutrition and Integrative Neurobiology (NutriNeuro), Bordeaux,
(2)UMR1286, Univ. Bordeaux, Nutrition et Neurobiologie Intégrée, Bordeaux,
(3)Toxalim UMR 1331, Groupe de Neurogastroentérologie and Nutrition, INRA,
INP-EI-Purpan, Univ. Toulouse, Toulouse, France.
(4)UMR1286, INRA, Nutrition and Integrative Neurobiology (NutriNeuro), Bordeaux,
(5)UMR1286, Univ. Bordeaux, Nutrition et Neurobiologie Intégrée, Bordeaux,
The medial prefrontal cortex (mPFC) is a key area for the regulation of numerous
brain functions including stress response and cognitive processes. This brain
area is also particularly affected by adversity during early life. Using an
animal model in rats, we recently demonstrated that maternal exposure to a
high-fat diet (HFD) prevents maternal separation (MS)-induced gene expression
alterations in the developing PFC and attenuates several long-term deleterious
behavioral effects of MS. In the present study, we ask whether maternal HFD could
protect mPFC neurons of pups exposed to early life stress by examining dendritic
morphology and spine density in juvenile [postnatal day (PND) 21] and adult rats
submitted to MS. Dams were fed either a control or an HFD throughout gestation
and lactation, and pups were submitted to MS from PND2 to PND14. We report that
maternal HFD prevents MS-induced spine loss at PND21 and dendritic atrophy at
adulthood. Furthermore, we show in adult MS rats that PFC-dependent memory
extinction deficits are prevented by maternal HFD. Finally, perinatal HFD
exposure reverses gut leakiness following stress in pups and seems to exert an
anti-stress effect in dams. Overall, our work demonstrates that maternal HFD
affects the developing brain and suggests that nutrition, possibly through
gut-brain interactions, could modulate mPFC sensitivity to early stress.