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September 7th, 2025
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Sorbonne University, CNRS, INSERM, Inbstitut de Biologie Paris Seine (IBPS), Center for Neuroscience at Sorbonne University (NeuroSU)
neuroscience
bioRxiv

Obesogenic Diet Impairs Social Memory Through Alterations of Hippocampal CA2 Excitability and Oxytocin Signaling

Muller, M.Open in Google Scholar•Fermigier, A.Open in Google Scholar•Ducourneau, E. G.Open in Google Scholar•Rakotonandrasana, A.Open in Google Scholar•Ferreira, G.Open in Google Scholar•Chevaleyre, V.Open in Google Scholar•Piskorowski, R. A.Open in Google Scholar

While obesity induces cardio-metabolic disorders and cognitive deficits, the underlying neural mechanisms remain unexplored. In mice, exposure to an obesogenic high-fat and sugar diet (HFD) resulted in social recognition memory deficits, a process that is dependent upon hippocampal area CA2 and oxytocin signaling. HFD-fed mice had stronger inputs onto CA2 pyramidal neurons that led to increased action potential firing, without altering intrinsic properties or inhibitory transmission. Chemogenetic CA2 inhibition rescued HFD-induced social memory deficits, confirming the role of CA2 hyperexcitability in these effects. In CA2, oxytocin receptor activation resulted in membrane depolarization, spontaneous action-potential firing and permitted endocannabinoid-mediated plasticity in control diet-fed mice, but not HFD-fed littermates. In a concentration-dependent manner, oxytocin restored potentiation of excitatory responses and allowed for endocannabinoid plasticity at CA2 inhibitory synapses as well as social memory deficits in HFD-fed mice. By investigating the influence of diet on hippocampal area CA2, this study uncovers novel mechanisms linking neuromodulation and plasticity in social memory encoding.

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