| Project/Area Number |
15590217
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Environmental physiology (including Physical medicine and Nutritional physiology)
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| Research Institution | Osaka Bioscience Institute |
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Principal Investigator |
EGUCHI Naomi (2004) Osaka Bioscience Institute, Department of Molecular Behavioral Biology, Vice-Head, 分子行動生物学部門, 研究副部長 (10250086)
坂田 三恵 (2003) (財)大阪バイオサイエンス研究所, 分子行動生物学部門, 研究員 (10353525)
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| Co-Investigator(Kenkyū-buntansha) |
SAKATA Mie Waseda University, Advanced Research Institute for Bioscience, Lecturer, 先端バイオ研究所, 講師 (10353525)
URADE Yoshihiro Osaka Bioscience Institute, Department of Molecular Behavioral Biology, Head, 分子行動生物学部門, 研究部長 (10201360)
SEI Hiroyoshi The University of Tokushima Graduate School, Institute of Health Biosciences, Department of Medical Informatics, Assistant Professor, 医学部・医学科・情報統合医学講座統合生理医学分野, 助教授 (40206602)
江口 直美 (財)大阪バイオサイエンス研究所, 分子行動生物学部門, 研究副部長 (10250086)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2004: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2003: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Rapid-eve movement sleep / Arterial pressure / Heart rate / Autonomic regulation / Adenosine / Dopamine / Adenosine A_<2A> receptor / ドーパミンD2受容体 |
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| Research Abstract |
Autonomic function such as arterial pressure (AP), heart rate (HR), and respiration is quite stable and show the constant value during non-rapid eye movement (non-REM) sleep, but significantly fluctuates during REM sleep. However, the central mechanism for AP and HR changes associated with REM sleep remains unclear. Adenosine is an endogenous sleep substance. Dopamine serves as an AP regulator. An antagonistic interaction between adenosine A_<2A> receptor (A_<2A>R) and dopamine D_2 receptor has been well known. In this study, we simultaneously recorded electroencepharogram (EEG), electromyogram (EMG), AP, and HR in wild-type and the A_<2A>R gene-knockout (KO) mice to clarify the role of A_<2A>R in REM sleep-related cardiovascular function.
An A_<2A>R agonist (CGS-21680) induced sleep as judged by EEG and EMG recordings. In vivo microdialysis revealed that this agonist inhibited histamine release in both the frontal cortex and medial pre-optic area in a dose-dependent manner, and increased GABA release specifically in the histaminergic tuberomammillary nucleus but not in the frontal cortex. These results suggest that the A_<2A>R agonist induced sleep by inhibiting the histaminergic arousal system through increasing GABA release.
In wild-type mice, mean AP decreased during REM sleep, transiently dropped at REM sleep-offset, and then recovered to the basal level. HR also decreased during REM sleep, quickly increased at REM sleep-offset, and then recovered to the basal level. On the other hand, in A_<2A> KO mice, both mean AP and HR remarkably increased during REM sleep and then decreased quickly at REM sleep-offset. These results, taken together, indicate that A_<2A>R is involved in the autonomic regulation during REM sleep.
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