Data from: Chemogenetic inhibition of the medial prefrontal cortex reverses the effects of REM sleep loss on sucrose consumption

Rapid eye movement (REM) sleep loss is associated with increased consumption of weight promoting foods. The prefrontal cortex (PFC) is thought to mediate reward anticipation. However, the precise role of the PFC in mediating reward responses to highly palatable foods (HPF) after REM sleep deprivation is unclear. We selectively reduced REM sleep in mice over a 25-48 h period and chemogenetically inhibited the medial PFC (mPFC) by using an altered glutamate and ivermectin (IVM) gated chloride channel (GluClαβ) that facilitated neuronal inhibition through hyperpolarizing infected neurons. HPF consumption was measured while the mPFC was inactivated and REM sleep loss was induced. We found that REM sleep loss increased HPF consumption compared to control animals. However, mPFC inactivation reversed the effect of REM sleep loss on sucrose consumption without affecting fat consumption. Our findings provide, for the first time, a causal link between REM sleep, mPFC function and HPF consumption.快速眼动（rapid eye movement，REM）睡眠剥夺与促进体重增长的食物摄入量升高存在关联。前额叶皮层（prefrontal cortex，PFC）被认为可介导奖赏预期，但REM睡眠剥夺后，PFC在介导机体对高适口性食物（highly palatable foods，HPF）的奖赏反应中的具体作用仍不明确。本研究在25至48小时内选择性减少小鼠的REM睡眠时间，并通过改造的谷氨酸与伊维菌素（ivermectin，IVM）门控氯离子通道（GluClαβ）化学遗传学抑制内侧前额叶皮层（medial PFC，mPFC）——该通道可通过超极化感染神经元实现神经抑制。我们在mPFC失活且REM睡眠剥夺被诱导的条件下，测定了HPF摄入量。结果显示，与对照组小鼠相比，REM睡眠剥夺提升了HPF摄入量；但mPFC失活可逆转REM睡眠剥夺对蔗糖摄入量的影响，却未对膳食脂肪摄入量产生作用。本研究首次为REM睡眠、mPFC功能与HPF摄入量之间的因果关联提供了实验依据。