| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 2016: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 2015: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2014: ¥900,000 (Direct Cost: ¥900,000)
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| Outline of Annual Research Achievements |
Human sleep proceeds in cycles. A greater amount of deep sleep is prevalent earlier in the night, while the proportion of REM sleep increases in the two cycles prior to natural awakening. It is not well understood what role REM sleep loss plays in affecting areas of the brain that control the desire to consume unhealthy foods. The prefrontal cortex (PFC) plays a role in judging the palatability of foods through taste, smell and texture. Moreover, persons who are obese tend to have increased activity in the PFC when exposed to high calorie foods. 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. In other words, the medial prefrontal cortex may play a direct role in controlling our desire to consume weight promoting foods, high in sucrose content, when we are lacking sleep, especially REM sleep.
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