| Summary: | Summary: 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. : State-dependent plasticity in neuronal circuits controlling hunger is well established. Nuzzaci et al. show that this process is recapitulated after a meal. Postprandial hyperglycemia induces glial retraction around hypothalamic POMC neurons, which increases the activity of these anorectic neurons. This macronutrient-dependent plasticity provides a neurobiological basis for satiety. Keywords: hypothalamus, plasticity, energy homeostasis, obesity, melanocortin system, pro-opiomelanocortin neurons, astrocytes, food intake, satiety
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