{'fraction_non_alphanumeric': 0.02664067576348278, 'fraction_numerical': 0.007147498375568551, 'mean_word_length': 5.581196581196581, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Bidirectional modulation of hippocampal and amygdala synaptic plasticity by post‐weaning obesogenic diet intake in male rats: Influence of the duration of diet exposure

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.