| 配分額 *注記 |
9,100千円 (直接経費: 7,000千円、間接経費: 2,100千円)
2018年度: 4,550千円 (直接経費: 3,500千円、間接経費: 1,050千円)
2017年度: 4,550千円 (直接経費: 3,500千円、間接経費: 1,050千円)
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| 研究実績の概要 |
It is widely accepted that sleep disruption affects metabolism and energy balance, but the neuronal mechanisms linking sleep disruption and obesity are poorly defined. Recent work from our lab suggests a role of neurons in the medial prefrontal cortex (mPFC) in linking REM sleep to appetite for highly palatable food (HPF). REM sleep is a unique phase of sleep in mammals that is characterized by random eye movement and low muscle tone throughout the body. The prefrontal cortex 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 prefrontal cortex when exposed to high calorie foods.
We also discovered that REM sleep is suppressed by activation of REM-active dopaminergic or GABAergic mesopontine neurons, suggesting that these neurons may control the level of REM sleep and/or executive functions during REM sleep. In addition, we found that activation of the GABAergic, but not the dopaminergic, mesopontine neurons strongly induced slow-wave sleep. We continue to elucidate a role of dopaminergic and GABAergic mesopontine neurons in linking REM sleep to HPF consumption.
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