2002 Fiscal Year Final Research Report Summary
TURNING POINT OF FUNCTIONAL RECOVERY AND SYNAPTIC MODULATION IN HUMAN MATURE BRAIN WITH BRAIN INJURY.
| Project/Area Number |
13470297
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | KYOTO PREFECTURAL UNIVERSITY OF MEDICINE |
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Principal Investigator |
IMAHORI Yoshio KYOTO PREFECTURAL UNIVERSITY OF MEDICINE, ASSOCIATE PROFESSOR., 医学部, 助教授 (80191899)
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| Co-Investigator(Kenkyū-buntansha) |
OWADA Kei KYOTO PREFECTURAL UNIVERSITY OF MEDICINE ASSISTANT PROFESSOR., 医学部, 助手 (80332948)
KIMURA Minoru KYOTO PREFECTURAL UNIVERSITY OF MEDICINE, PROFESSOR., 医学部, 教授 (40118451)
MINEURA Katsuyoshi KYOTO PREFECTURAL UNIVERSITY OF MEDICINE, PROFESSOR., 医学部, 教授 (70134103)
TATSUZAWA Kazunori KYOTO PREFECTURAL UNIVERSITY OF MEDICINE ASSISTANT PROFESSOR., 医学部, 助手 (80347450)
TSUJINO Hitoshi KYOTO PREFECTURAL UNIVERSITY OF MEDICINE ASSISTANT PROFESSOR., 医学部, 助手 (00347452)
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| Project Period (FY) |
2001 – 2002
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| Keywords | positron emission tomography / network plasticity / neuronal plasticity / phosphoinositide turnover / C-11標識1,2-diacylglycerol / 大脳連合野 / 前頭前野 / protein kinase C |
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| Research Abstract |
Functional recovery is caused by the modulation of synaptic transmission in the damaged brain. Major turning point in functional recovery is based on synergic action of network plasticity and neuronal plasticity. The synaptic modulations newly reorganize optimal networks and establish stabilized functional units. We have developed the method using PET in order to know this modulation function in the human brain by visualization of second messenger system. Higher brain function recovery mechanism was examined using this method for the relation between enhancement of phosphoinositide turnover and an improvement of higher brain function. In the case in which the enhancement appeared in the region of which the plastic function of front association area is strong, there was functional recovery. We adopted rat experimental model with brain injury because of reproducible phenomenon. Confocal laser microscope and fluorescent labeling DAG were newly synthesized. As a result of examining the localization of the enhancement phenomenon by the micro level, it occurred in the dendrite. The dyeing agreed with the position of the enhancement in the immunohistochemical technique using the CaMKII-active antibody and PKC. This suggests the stage in the alteration of the phospholipid membrane structure. As a result of imaging of phosphoinositide turnover in the direct human, the existence of reinforcement of the phospholipid signal clarified in the synaptic modulations. In conclusion mature brain was reorganized by synergic action of network plasticity and neuronal plasticity and the whole brain supported this action, especially in the region of the prefrontal association cortex.
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[Publications] Nakazawa N, Wakita K, Mineura K, Nakamura M, Fujii R, Nakanishi H, Uji Y, Matsuura S, Itani K, Kanatsuna T, Ido T, Imahori Y.: "Short time bacterial endotoxins test for positron emission tomography by means of positively charged filters"Kaku Igaku. 39(4). 543-548 (2002)
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「研究成果報告書概要(欧文)」より
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[Publications] Kagaya Y, Chida M, Imahori Y, Fujii R, Namiuchi S, Takeda M, Yamane Y, Otani H, Watanabe J, Fukuchi M, Tezuka F, Ido T, Shirato K.: "Effect of angiotensin converting enzyme inhibition on myocardial phosphoinositide metabolism visualised with 1-[1-11C]-butyry1-2-palmitoyl-rac-glycerol in myocardial infarction in the rat"Eur J Nucl Med Mol Imaging. 29(11). 1516-1522 (2002)
Description
「研究成果報告書概要(欧文)」より
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