| Project/Area Number |
11470318
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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 |
Anesthesiology/Resuscitation studies
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| Research Institution | NIIGATA UNIVERSITY |
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Principal Investigator |
TAGA Kiichiro NIIGATA UNIVERSITY, Graduate School of Medical and Dental Sciences Associate Professor, 大学院・医歯学総合研究科, 助教授 (00163329)
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| Co-Investigator(Kenkyū-buntansha) |
SATO Kazunori NIIGATA UNIVERSITY, Medical Hospital Lecturer, 医学部・附属病院, 講師 (70126415)
FUJIWARA Naoshi NIIGATA UNIVERSITY, Faculty of Medicine Associate Professor, 医学部, 助教授 (70181419)
渡辺 逸平 新潟大学, 医学部・附属病院, 助手 (00251819)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥14,200,000 (Direct Cost: ¥14,200,000)
Fiscal Year 2001: ¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 2000: ¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1999: ¥8,800,000 (Direct Cost: ¥8,800,000)
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| Keywords | cerebral ischemia / ischemic tolerance / voltage sensitive dye / near infrared / video-enhanced / hippocampal slice / propagation of membrane depolarization / membrane potential / MAP-2 / 樹状突起 / ビデオエンハンス |
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| Research Abstract |
1) The effects of cortical spreading depression (CSD) and anesthetics on the induction of ischemic tolerance were investigated. Non-fasted male Wistar rats were used. Volatile anesthetics, halothane, isoflurane and sevoflurane induced suppression of CSD elicitaion in a dose dependent manner. With increasing concentrations of each volatile anesthetic, there was dose-related reduction in CSD frequency but not in CSD amplitude. However, volatile anesthetics isoflurane and sevoflurane did not have any effect on the signal transduction pathways that lead to c-fos expression.
2) Using the optical recording techniques with voltage sensitive dyes, we investigated the functional integrity of the hippocampus in gerbils that had undergone ischemic preconditioning with that in gerbils that were not preconditioned. Non-fasted male Mongolian gerbils were used. In the ischemia group, both carotid arteries were occluded for 5 min. In the tolerance group, forebrain ischemia was produced for 2 min (ische
… More
mic preconditioning).
The animals were then subjected to forebrain ischemia for a period of 5 min 24 h after ischemic preconditioning.
Hippocampal slices were prepared 1 day, Sweeks and 6 months after 5 min ischemia. In these slices, the propagation of membrane depolarization across the hippocampus in response to electrical stimulation of CA1 was monitored. In the control group, electrical stimulation of the stratum radiatum resulted in a rapid depolarization of the tissue at the site of stimulation. This depolarization then spread across the hippocampus, leading to the depolarization of the stratum oriens. In*the ischemia group, propagation and duration of the depolarization was significantly depressed and shorter with all recovery times than control. In the tolerance group, both the extent of propagation and the duration of depolarization were reduced slightly in comparison to control slices. These findings were observed 1 day and 8 weeks after ischemia. They were still evident 6 months after ischemia. These results suggest that neurons that had undergone ischemic preconditioning preserve propagation of membrane depolarization for long recovery period. Less
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