| Project/Area Number |
21590740
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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 |
Legal medicine
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
YOSHIMOTO Kanji 京都府立医科大学, 医学研究科, 准教授 (70111903)
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| Co-Investigator(Kenkyū-buntansha) |
NISHIMURA Akira 京都府立医科大学, 医学研究科, 講師 (00360040)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2010: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2009: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | 虚血 / 再灌流障害 / ドパミン / セロトニン / ロテノン / アルコール医学 / 脳虚血 / 脳報償系 / アルコール / in vivo |
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| Research Abstract |
In the present study, we used in vivo brain microdialysis to examine the effects of stimulations of ischemia and/or potassium on the release of dopamine(DA) and serotonin(5-HT) in the nucleus accumbens(ACC)) of anesthetized rats. Ischemia(Four vessels occlusion : 4VO) for 10 min increased DA and 5-HT release in the ACC 200-fold and 15-fold, respectively, in the first experiment. In second experiment, releases of DA and 5-HT in the ACC increased 350-400% and 150-180% by first and second K^+stimulation, respectively, in the K^+-K^+group. The 4VO treatment induced significant and massive increases of DA and 5-HT releases in the ACC, following K^+stimulation increased 5-HT release significantly in the Ischemia-K^+group compared with the K^+-K^+group. Although second K^+stimulation increased DA release in the both group, but it was not significant changes in DA releases. K^+-induced ACC 5-HT release was higher in the ischemia-treated rats than non ischemia-treated rats. Different brain vuln
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erability was shown in the dopaminergic and serotonergic neurons in the ACC following the ischemic treatment. These findings suggested that the mesolimbic neurons indicated a resistance to dysfunction associated with 10 min-ischemia and maintained neural function, monoamine synthesis and neurotransmitter releases, within the transient neural damage. Supplement data : The mice treated with rotenone showed increases in alcohol drinking behavior. Levels of DA and 5-HT in the ACC and C/P of chronic rotenone-treated mice were decreased, while the ratios of DOPAC to DA in the ACC and C/P and of 5HIAA to 5-HT in the ACC, C/P and DRN were increased significantly. Tyrosine hydroxylase immunoreactivity of chronic rotenone-treated mice(10 mg/kg, p. o.) slightly were decreased in both the striatum and the substatia nigra. Ethanol and acetaldehyde metabolism was not significantly different between mice treated with rotenone(10 mg/kg, p. o.) and controls. It was suggested that rotenone-treated mice had increased alcohol drinking behavior associated with increases in the DA turnover ratios of ACC and striatum to compensate for the neural degeneration. Less
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