Bidirectional modulation of hippocampal and amygdala synaptic plasticity by post‐weaning obesogenic diet intake in male rats: Influence of the duration of diet exposure
Hippocampus. 2020-11-04; :
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Vouimba RM(1)(2), Bakoyiannis I(1)(3), Ducourneau EG(1)(3), Maroun M(4), Ferreira G(1)(3).
(1)Université de Bordeaux, Bordeaux Neurocampus, Bordeaux, France.
(2)CNRS, Institut de Neurosciences Cognitives et Intégratives d’Aquitaine, UMR 5287, Bordeaux, France.
(3)INRAE, Nutrition and Integrative Neurobiology, UMR 1286, Bordeaux, France.
(4)Sagol Department of Neurobiology, Faculty of Natural Sciences, University of Haifa, Haifa, Israel.
Obesity is a chronic condition associated with adverse memory and emotional
outcomes in humans and animal models. We have recently demonstrated that
post-weaning (i.e., periadolescent) high-fat diet (HFD)-induced obesity has
opposite effect on hippocampal and amygdala-dependent memory in rodents: while
HFD consumption impairs spatial and relational memory, it enhances cue-dependent
emotional memory. However, it is still not clear whether this bidirectional HFD
effect on memory is related to bidirectional alterations of hippocampal and
amygdala synaptic plasticity and if it is influenced by the duration of diet
intake. In the current study, we compared in male rats the impact of 2-3 and 6-7
months of HFD intake starting at weaning, thus covering adolescence, on in vivo
long-term potentiation (LTP) recorded simultaneously in the hippocampal area CA1
and the basolateral amygdala (BLA). As expected, 6-7 months of HFD intake
abolished LTP in the CA1 and enhanced LTP in the BLA. However, 2-3 months of of
HFD exposure enhanced LTP in both CA1 and BLA suggesting a transient compensatory
mechanism in hippocampus. These results indicate that post-weaning HFD intake
progressively leads to bidirectional modulation of hippocampal and amygdala
synaptic plasticity, as we previously demonstrated for related memory processes,
yet with a different temporal dynamic.