Acute exposure to a high-fat diet in juvenile male rats disrupts hippocampal-dependent memory and plasticity through glucocorticoids.

Tala Khazen, Ossama A. Hatoum, Guillaume Ferreira, Mouna Maroun
Sci Rep. 2019-08-22; 9(1):
DOI: 10.1038/s41598-019-48800-2

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Author information:
(1)Sagol Department of Neurobiology, Faculty of Natural Sciences, University of Haifa, Haifa, 3498838, Israel.
(2)Department of Surgery B- HaEmek Medical Center, Faculty of Medicine, Technion: Israel Institute of Technology, Haifa, Israel.
(3)INRA, Nutrition and Integrative Neurobiology, UMR1286, Bordeaux, France.
(4)University of Bordeaux, Nutrition and Integrative Neurobiology, UMR 1286, Bordeaux, France.
(5)Sagol Department of Neurobiology, Faculty of Natural Sciences, University of Haifa, Haifa, 3498838, Israel. .

The limbic circuit is still undergoing maturation during juvenility and adolescence, explaining why environmental and metabolic challenges during these
developmental periods can have specific adverse effects on cognitive functions. We have previously shown that long-term exposure (8-12 weeks) to high-fat diet (HFD) during adolescence (from weaning to adulthood), but not at adulthood, was associated with altered amygdala and hippocampal functions. Moreover, these HFD effects were normalized by treatment with glucocorticoid receptor (GR) e exposure (7-9 days) to HFD during juvenility [from postnatal day (PND) 21 to PND 28-30] or adulthood (from PND 60 to PND 67-69) is sufficient to affect hippocampal functions and whether it is also dependent on GRs activation. Juvenile HFD abolished both hippocampal synaptic plasticity, assessed through in vivo long-term potentiation (LTP) in CA1, and long-term hippocampal-dependent memory, using object location memory (OLM). No effect of HFD was observed in short-term OLM suggesting a specific effect on consolidation process. In contrast, adult HFD enhanced in vivo LTP and OLM. Systemic application of GR antagonist alleviated HFD-induced LTP and OLM impairments in juveniles. These results suggest that acute exposure to HFD during juvenility is sufficient to impair hippocampal functions in a GR-dependent manner. Interestingly, this effect depends on the developmental period studied as acute exposure to HFD at adulthood did not impair, but rather enhanced, hippocampal functions.


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