| Project/Area Number |
10680719
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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 |
Neurochemistry/Neuropharmacology
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| Research Institution | EHIME UNIVERSITY |
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Principal Investigator |
NAKAMURA Yoichi School of Medicine, Ehime Univ., Assistant Professor, 医学部, 助手 (90180413)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 1999: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1998: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | microglia / astrocytes / opioids / naloxone / db-cAMP / cytokines / enkephalin / endorphin / アストロサイト / オビオイド / 一酸化窒素 / 画像解析 |
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| Research Abstract |
There are many evidences indicating the interaction between central nervous system (CNS) and immune system. Microglia play major roles of immunological function in CNS and it is a very important approaches to elucidate their function including the interaction to astrocytes. We examined the effects of various opioids and the other compounds on the LPS-induced NO production from cultured microglia and astrocytes. The effect of opioids varied from cell preparations to preparations suggesting that endogenous opioids may be released into culture media and its extent varies under cell culture conditions. We examined the effect of naloxone, an opioid antagonist. Naloxone inhibited dose-dependently NO production from microglia but not from astrocytes. The inhibition was reversed by Met-enkephalin remarkably and β-endorphin slightly.
Among the other compounds examined, very interesting effects were observed in dibutyryl-cAMP, a membrane permeable analog, and propentofilline, a xanthine analoge. They showed almost no effect on LPS-induced production of NO and IL-6 ; however, they strongly inhibited LPS-induced production of TNF-α and IL-1β. The differential inhibition of cytokines production suggests that a possible control of microglial activation protects neuronal damage. Further investigation may provide a beneficial tool against neurodegenerative central diseases.
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