Abstract
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 glutamategated 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.
| Original language | English |
|---|---|
| Article number | e20269 |
| Journal | eLife |
| Volume | 5 |
| Issue number | DECEMBER2016 |
| DOIs | |
| Publication status | Published - 2016 Dec 6 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Neuroscience(all)
- Biochemistry, Genetics and Molecular Biology(all)
- Immunology and Microbiology(all)
Cite this
Chemogenetic inhibition of the medial prefrontal cortex reverses the effects of REM sleep loss on sucrose consumption. / McEown, Kristopher Scott; Takata, Yohko; Cherasse, Yoan; Nagata, Nanae; Aritake, Kosuke; Lazarus, Michael.
In: eLife, Vol. 5, No. DECEMBER2016, e20269, 06.12.2016.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Chemogenetic inhibition of the medial prefrontal cortex reverses the effects of REM sleep loss on sucrose consumption
AU - McEown, Kristopher Scott
AU - Takata, Yohko
AU - Cherasse, Yoan
AU - Nagata, Nanae
AU - Aritake, Kosuke
AU - Lazarus, Michael
PY - 2016/12/6
Y1 - 2016/12/6
N2 - 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 glutamategated 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.
AB - 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 glutamategated 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.
UR - http://www.scopus.com/inward/record.url?scp=85006043670&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85006043670&partnerID=8YFLogxK
U2 - 10.7554/eLife.20269
DO - 10.7554/eLife.20269
M3 - Article
VL - 5
JO - eLife
JF - eLife
SN - 2050-084X
IS - DECEMBER2016
M1 - e20269
ER -