Centre des Sciences du Goût et de l'Alimentation, AgroSup Dijon, CNRS, INRAE, Université Bourgogne Franche-Comté, 21000 Dijon, France.
Université Côte d'Azur, CNRS, Institut de Pharmacologie Moléculaire et Cellulaire, 06560 Valbonne, France.
Cell Rep. 2020 Mar 3;30(9):3067-3078.e5. doi: 10.1016/j.celrep.2020.02.029.
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.
在啮齿动物中的机制研究表明，控制食物摄入的神经元回路中存在突触重塑。然而，这一过程的生理相关性尚不清楚。在这里，我们发现下丘脑饱腹神经元 POMC 的放电活动在标准餐后增加。POMC 神经元餐后过度活跃依赖于涉及突触前机制的突触可塑性，而不涉及突触的结构重塑，而是胶质细胞覆盖的回缩。这些功能和形态神经胶质变化是由餐后高血糖引发的。化学诱导的 POMC 神经元上的神经胶质回缩足以增加 POMC 活性并改变进食模式。这些发现表明，黑皮质素系统内的突触可塑性发生在进食的时间尺度内，可能有助于短期控制食物摄入。有趣的是，高脂肪餐后这些效应消失，提示 POMC 神经元的神经胶质可塑性参与了食物的饱腹感特性。
