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

• Published in: eLife Vol. 5
• Main Authors: McEown, Kristopher, Takata, Yohko, Cherasse, Yoan, Nagata, Nanae, Aritake, Kosuke, Lazarus, Michael
• Format: Journal Article
• Language: English
• Published: England eLife Science Publications, Ltd 06-12-2016; eLife Sciences Publications Ltd; eLife Sciences Publications, Ltd
• Subjects: Animals; Appetite; Appetite Regulation; Brain; Chloride Channels - genetics; Chloride Channels - metabolism; Electroencephalography; Eye movements; Food; Food consumption; Glutamates - metabolism; Ivermectin; Ivermectin - metabolism; Light; Male; Mice, Inbred C57BL; Neuroscience; paradoxical sleep; Physiological aspects; Prefrontal cortex; Prefrontal Cortex - physiology; Recombinant Proteins - genetics; Recombinant Proteins - metabolism; Reinforcement; REM sleep; reward anticipation; Rodents; Short Report; Sleep deprivation; Sleep, REM; Sucrose; Sucrose - metabolism; Sweetening Agents - metabolism; paradoxical sleep; mouse; reward anticipation; neuroscience; prefrontal cortex; appetite; REM sleep
• ISSN: 2050-084X; 2050-084X
• DOI: 10.7554/elife.20269

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.