Journal
CELL REPORTS
Volume 30, Issue 9, Pages 3067-+Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2020.02.029
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Funding
- Agence National pour la Recherche (ANR) [ANR-13JSV1-0003-01]
- French Investissements d'Avenir'' program, project ISITE-BFC [ANR-15-IDEX-0003]
- Re' gion Bourgogne grant FEDER 2010 [O0431SGO003S03440]
- IDEX UCA Academia 3 program
- Fondation de la Recherche Medicale/Equipe [FRM DEQ20150331738]
- ANR Investments for the Future'' LABEX SIGNALIFE program [ANR-11-LABX-0028_01]
- FRM Camille Woringer Award 2016
- CAPES/COFECUB [Sv 848-15]
- FRM [DRM20101220421]
- Medisite Foundation award 2017
- Continuous Glucose Telemetry Award 2018 - Data Sciences International
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Mechanistic studies in rodents evidenced synaptic remodeling in neuronal circuits that control food intake. However, the physiological relevance of this process is not well defined. Here, we show that the firing activity of anorexigenic POMC neurons located in the hypothalamus is increased after a standard meal. Postprandial hyperactivity of POMC neurons relies on synaptic plasticity that engages pre-synaptic mechanisms, which does not involve structural remodeling of synapses but retraction of glial coverage. These functional and morphological neuroglial changes are triggered by postprandial hyperglycemia. Chemogenetically induced glial retraction on POMC neurons is sufficient to increase POMC activity and modify meal patterns. These findings indicate that synaptic plasticity within the melanocortin system happens at the timescale of meals and likely contributes to short-term control of food intake. Interestingly, these effects are lost with a high-fat meal, suggesting that neuroglial plasticity of POMC neurons is involved in the satietogenic properties of foods.
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