Chemogenetic inhibition of the medial prefrontal cortex reverses the effects of REM sleep loss on sucrose consumption
Chemogenetic inhibition of the medial prefrontal cortex reverses the effects of REM sleep loss on sucrose consumption
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DOI：
10.7554/elife.20269
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发表时间：
2016-12
期刊：
影响因子：
7.7
通讯作者：
K. McEown;Yohko Takata;Y. Chérasse;N. Nagata;K. Aritake;M. Lazarus
中科院分区：
文献类型：
--
作者：
K. McEown;Yohko Takata;Y. Chérasse;N. Nagata;K. Aritake;M. Lazarus
快速眼动（REM）睡眠缺失与促进体重的食物摄入增加有关。前额叶皮层（PFC）被认为是调节奖励预期的。然而，在快速眼动睡眠剥夺后，PFC在调节对美味食物（HPF）的奖励反应中的确切作用尚不清楚。我们选择性地减少小鼠在25-48小时内的快速眼动睡眠，并通过改变谷氨酸门控和伊维菌素门控的氯通道来抑制内侧PFC (mPFC)，从而促进通过超极化感染神经元的神经元抑制。在mPFC失活和REM睡眠缺失的情况下测量HPF消耗。我们发现，与对照动物相比，快速眼动睡眠的缺失增加了HPF的消耗。然而，mPFC失活逆转了快速眼动睡眠缺失对蔗糖消耗的影响，而不影响脂肪消耗。我们的发现首次提供了REM睡眠、mPFC功能和HPF消耗之间的因果关系。DOI: http://dx.doi.org/10.7554/eLife.20269.001
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 hr period and chemogenetically inhibited the medial PFC (mPFC) by using an altered glutamate-gated and ivermectin-gated chloride channel 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. DOI: http://dx.doi.org/10.7554/eLife.20269.001