| Budget Amount *help |
¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2019: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2018: ¥800,000 (Direct Cost: ¥800,000)
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| Outline of Annual Research Achievements |
Mammalian sleep is composed of rapid-eye-movement (REM) sleep and non-REM (NREM) sleep. REM sleep is particularly susceptible to various external factors or diseases. Although several genes are associated with REM sleep, the relationship between the products of these genes and the brain areas critical for regulating REM sleep remains poorly understood. Moreover, the molecular mechanisms underlying changes in REM sleep caused by environmental factors are unclear. Here, I focused on Cpne7, as a gene that is highly expressed in the sublateral dorsal nucleus (SLD), a brain area critical for generating REM sleep in rodents. The function of the product of Cpne7, copine-7 in the brain was unknown. Therefore, I generated a Cpne7-Cre knock-in mouse line that allows us to examine the effect of deleting Cpne7 and to genetically label and manipulate cells that express Cpne7. As a results, I found the baseline sleep was not changed in Cpne7-KO mice. However, the amount of REM sleep was more in Cpne7-KO mice following cage change or water immersion and restraint stress, both of which are conditions that acutely reduce REM sleep, suggesting copine-7 is involved in the regulation of REM sleep under certain conditions. Moreover, chemogenetic activation of Cpne7-expression neurons in the SLD reduced the amount of REM sleep, suggesting these neurons negatively regulate REM sleep. Collectively, these results suggest copine-7 and Cpne7-expressing neurons in the SLD as candidate molecular or neuronal components of the regulatory system that controls REM sleep.
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