Chronic hyperpalatable diet induces impairment of hippocampal-dependent memories and alters glutamatergic and fractalkine axis signaling
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Published:2023-09-29
Issue:1
Volume:13
Page:
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ISSN:2045-2322
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Container-title:Scientific Reports
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language:en
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Short-container-title:Sci Rep
Author:
Ribeiro Roberta,Silva Emanuele Guimarães,Moreira Felipe Caixeta,Gomes Giovanni Freitas,Cussat Gabriela Reis,Silva Barbara Stehling Ramos,da Silva Maria Carolina Machado,de Barros Fernandes Heliana,de Sena Oliveira Carolina,de Oliveira Guarnieri Leonardo,Lopes Victoria,Ferreira Cláudia Natália,de Faria Ana Maria Caetano,Maioli Tatiani Uceli,Ribeiro Fabíola Mara,de Miranda Aline Silva,Moraes Grace Schenatto Pereira,de Oliveira Antônio Carlos Pinheiro,Vieira Luciene Bruno
Abstract
AbstractChronic consumption of hyperpalatable and hypercaloric foods has been pointed out as a factor associated with cognitive decline and memory impairment in obesity. In this context, the integration between peripheral and central inflammation may play a significant role in the negative effects of an obesogenic environment on memory. However, little is known about how obesity-related peripheral inflammation affects specific neurotransmission systems involved with memory regulation. Here, we test the hypothesis that chronic exposure to a highly palatable diet may cause neuroinflammation, glutamatergic dysfunction, and memory impairment. For that, we exposed C57BL/6J mice to a high sugar and butter diet (HSB) for 12 weeks, and we investigated its effects on behavior, glial reactivity, blood–brain barrier permeability, pro-inflammatory features, glutamatergic alterations, plasticity, and fractalkine-CX3CR1 axis. Our results revealed that HSB diet induced a decrease in memory reconsolidation and extinction, as well as an increase in hippocampal glutamate levels. Although our data indicated a peripheral pro-inflammatory profile, we did not observe hippocampal neuroinflammatory features. Furthermore, we also observed that the HSB diet increased hippocampal fractalkine levels, a key chemokine associated with neuroprotection and inflammatory regulation. Then, we hypothesized that the elevation on glutamate levels may saturate synaptic communication, partially limiting plasticity, whereas fractalkine levels increase as a strategy to decrease glutamatergic damage.
Funder
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior Programa de Apoio à Pós-graduação Conselho Nacional de Desenvolvimento Científico e Tecnológico Fundação de Amparo à Pesquisa do Estado de Minas Gerais Pró-Reitoria de Pesquisa, Universidade Federal de Minas Gerais
Publisher
Springer Science and Business Media LLC
Subject
Multidisciplinary
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