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 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.