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Mol Neurobiol ; 59(8): 4902-4925, 2022 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-35657456

RESUMO

Evidence has accumulated that higher consumption of high-fat diets (HFDs) during the juvenile/adolescent period induces altered hippocampal function and morphology; however, the mechanism behind this phenomenon remains elusive. Using high-resolution structural imaging combined with molecular and functional interrogation, a murine model of obesity treated with HFDs for 12 weeks after weaning mice was shown to change in the glutamate-mediated intracellular calcium signaling and activity, including further selective reduction of gray matter volume in the hippocampus associated with memory recall disturbance. Dysregulation of intracellular calcium concentrations was restored by a non-competitive α-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) antagonist, followed by normalization of hippocampal volume and memory recall ability, indicating that AMPARs may serve as an attractive therapeutic target for obesity-associated cognitive decline.


Assuntos
Receptores de AMPA , Receptores de N-Metil-D-Aspartato , Animais , Cálcio/metabolismo , Hipocampo/metabolismo , Camundongos , Obesidade , Permeabilidade , Receptores de AMPA/metabolismo , Receptores de N-Metil-D-Aspartato/metabolismo
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