Early‐life and chronic exposure to high‐fat diet alters noradrenergic and glutamatergic neurotransmission in the male rat amygdala and hippocampus under cognitive challenges
Childhood obesity increases the risk of health and cognitive disorders in adulthood. Consuming high‐fat diets (HFD) during critical neurodevelopmental periods, like childhood, impairs cognition and memory in humans and animals, affecting the function and connectivity of brain structures related to e...
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Published in | Journal of neuroscience research Vol. 102; no. 6; pp. e25360 - n/a |
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Main Authors | , , , , , , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Wiley Subscription Services, Inc
01.06.2024
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Subjects | |
Online Access | Get full text |
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Summary: | Childhood obesity increases the risk of health and cognitive disorders in adulthood. Consuming high‐fat diets (HFD) during critical neurodevelopmental periods, like childhood, impairs cognition and memory in humans and animals, affecting the function and connectivity of brain structures related to emotional memory. However, the underlying mechanisms of such phenomena need to be better understood. This study aimed to investigate the neurochemical profile of the amygdala and hippocampus, brain structures involved in emotional memory, during the acquisition of conditioned odor aversion in male rats that consumed a HFD from weaning to adulthood. The rats gained weight, experienced metabolic changes, and reduced insulin sensitivity and glucose tolerance. Rats showed enhanced odor aversion memory, contrary to the expected cognitive impairments. This memory enhancement was accompanied by increased noradrenergic and glutamatergic neurotransmission in the amygdala and hippocampus. Importantly, this upregulation was specific to stimuli exposure, as basal neurotransmitter levels remained unaltered by the HFD. Our results suggest that HFD modifies cognitive function by altering neurochemical signaling, in this case, upregulating neurotransmitter levels rendering a stronger memory trace, demonstrating that metabolic dysfunctions do not only trigger exclusively detrimental plasticity processes but also render enhanced plastic effects depending on the type of information.
High‐fat diets alter amygdala and hippocampus neurochemistry in juvenile male rats. Rats with metabolic changes show enhanced odor aversion memory, linked to elevated noradrenergic and glutamatergic neurotransmission. This highlights intricate connections between obesogenic diets, neurochemistry, and cognition, implying that metabolic dysfunctions can induce both detrimental and enhanced plasticity effects. |
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Bibliography: | Consortium author list recognizes the significant and irreducible commitment with the conceptualization, management, and realization of this research project. OBEETEEN Consortium: Guillaume Ferreira (Univ. Bordeaux, INRAE, Bordeaux INP, Nutrition and Integrative Neurobiology, UMR 1286, Bordeaux, France), Gustavo Pacheco‐Lopez (Health Sciences Department, Metropolitan Autonomous University (UAM), Campus Lerma, Lerma, Mexico), Etienne Coutureau (Univ. Bordeaux, CNRS, INCIA, UMR 5287, Bordeaux, France), Ranier Gutierrez (Department of Pharmacology, Center for Research and Advanced Studies (CINVESTAV), Mexico City, Mexico), Pascal Barat (Univ. Bordeaux, INRAE, Bordeaux INP, Nutrition and Integrative Neurobiology, UMR 1286, Bordeaux, France; CHU Bordeaux, Children hospital, Bordeaux, France), Federico Bermudez‐Rattoni (Cellular Physiology Institute, National Autonomous University of Mexico (UNAM), Mexico City, Mexico), Gwenaelle Catheline (Univ. Bordeaux, CNRS, INCIA, UMR 5287, Bordeaux, France), Claudia I. Pérez (Department of Pharmacology, Center for Research and Advanced Studies (CINVESTAV), Mexico City, Mexico), Pauline Lafenêtre (Univ. Bordeaux, INRAE, Bordeaux INP, Nutrition and Integrative Neurobiology, UMR 1286, Bordeaux, France), Daniel Osorio‐Gomez (Cellular Physiology Institute, National Autonomous University of Mexico (UNAM), Mexico City, Mexico), Kioko Guzman‐Ramos (Health Sciences Department, Metropolitan Autonomous University (UAM), Campus Lerma, Lerma, Mexico), Fabien Naneix (Univ. Bordeaux, INRAE, Bordeaux INP, Nutrition and Integrative Neurobiology, UMR 1286, Bordeaux, France; Univ. Bordeaux, CNRS, INCIA, UMR 5287, Bordeaux, France), Ernesto Sanz‐Arigita (Univ. Bordeaux, INRAE, Bordeaux INP, Nutrition and Integrative Neurobiology, UMR 1286, Bordeaux, France; Univ. Bordeaux, CNRS, INCIA, UMR 5287, Bordeaux, France), Ioannis Bakoyiannis (Univ. Bordeaux, INRAE, Bordeaux INP, Nutrition and Integrative Neurobiology, UMR 1286, Bordeaux, France). Edited by Cristina Antonella Ghiani and Lindsay R. Halladay. Reviewed by Miriam Ribeiro and Joana Margarida Gaspar. Note ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0360-4012 1097-4547 |
DOI: | 10.1002/jnr.25360 |