Establishment of molecular mechanism of exercise motivation using a novel rat-strain featured by high levels of wheel-running activity
Establishment of molecular mechanism of exercise motivation using a novel rat-strain featured by high levels of wheel-running activity
批准号:
21700696
负责人:
MORISHIMA Masaki
金额:
$2.25万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Young Scientists (B)
财政年份:
2009
资助国家:
日本
项目状态:
已结题
起止时间:
2009 至 2011
中文摘要
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英文摘要
We established a novel rat strain featured by high levels of voluntary wheel-running, which is called SPORTS(Spontaneously-Running Tokushima-Shikoku) rat. The aim of this study was to investigate the effect of high-or low-intensities in voluntary exercise on sympathetic and vagal controls of heart at sedentary and during wheel-running exercise by use of SPORTS rats. At 15 weeks of age, each rat was moved to a new cage with or without an exercise wheel, and sorted into four groups ; 1) SPORTS rat with an exercise wheel(running), 2) SPORTS rat without an exercise wheel(sedentary), 3) control rat with an exercise wheel(running), and 4) control rat without an exercise wheel(sedentary). Heart rate was significantly increased in sedentary SPORTS rats compared to those in control rats. SPORTS rats show a significant reduction in resting heart rate by high-intensity running. The low frequency/high frequency(LF/HF) ratio, which reflects cardiac sympathetic nerve activity, was significantly decreased in SPORTS rats by voluntary running. However, a decrease of sympathetic nerve activity was not observed in control rats with approximately 1/10 wheel-running activity. By wheel running, the low frequency(LF) power was augmented in control rats, and was markedly depressed in SPORTS rats. High-intensity voluntary running decreases mean heart rate during resting period(sedentary) with a depression of sympathetic nerve activity. These results suggest that high-intensity voluntary exercise attenuates sympathetic nerve activity not only during exercise but also during resting period as a lasting effects.
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替米沙坦抑制心肌细胞T型钙离子通道的表达
DOI:
--
发表时间:
2009
期刊:
European Journal of Pharmacology 609(1-3)
影响因子:
--
作者:
[森島真幸, 王岩, 秋吉裕子, 宮本伸二, 小野克重]
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小野克重
Trancription factor Csx/Nkx2. 5 and NFAT regulate expression of Ca_V3. 2 T-type Ca^<2+> channel via protein kinase Cactions
转录因子Csx/Nkx2。
DOI:
--
发表时间:
2010
期刊:
影响因子:
--
作者:
[Katushige Ono, Masaki Morishima, Yan Wang]
通讯作者:
Yan Wang
DOI:
10.1016/j.ejphar.2009.03.024
发表时间:
2009-05
期刊:
European journal of pharmacology
影响因子:
5
作者:
[M. Morishima;Yan Wang;Yuko Akiyoshi;S. Miyamoto;K. Ono]
通讯作者:
M. Morishima;Yan Wang;Yuko Akiyoshi;S. Miyamoto;K. Ono
ノナペプチドであるOxytocinとVasopressinはCav1.2-L型カルシウムイオンチャネルの発現を制御する
九肽催产素和加压素调节Cav1.2-L型钙离子通道的表达
DOI:
--
发表时间:
2010
期刊:
Journal of Arrhythmia (掲載確定)(未定)
影响因子:
--
作者:
[森島真幸, 田原慎太郎, 王岩, 賀来俊彦, 小野克重]
通讯作者:
小野克重
アンジオテンシン受容体を介した心筋T型カルシウムチャネルの発現抑制
通过血管紧张素受体抑制心脏 T 型钙通道表达
DOI:
--
发表时间:
2010
期刊:
影响因子:
--
作者:
[森島真幸, 王岩, 秋吉裕子, 小野克重]
通讯作者:
小野克重
共 16 条
MicroRNA overexpression to establish a new arrhythmia model for studying its molecular mechanism(Fostering Joint International Research)
-
批准号:15KK0313
-
项目类别:Fund for the Promotion of Joint International Research (Fostering Joint International Research)
-
资助金额:$7.65万
-
财政年份:2016
-
负责人:MORISHIMA Masaki
-
依托单位:
MicroRNA overexpression to establish a new arrhythmia model for studying its molecular mechanism.
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批准号:15K08179
-
项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.91万
-
财政年份:2015
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负责人:MORISHIMA Masaki
-
依托单位:
Establishment of neural factor for regulating exercise activity and cardiac hypertrophy
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批准号:24700754
-
项目类别:Grant-in-Aid for Young Scientists (B)
-
资助金额:$2.66万
-
财政年份:2012
-
负责人:MORISHIMA Masaki
-
依托单位:
海外基金