1990 Fiscal Year Final Research Report Summary
Studies on the neural functions of platelet-activating factor
| Project/Area Number |
01571019
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Functional basic dentistry
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
DOHI Toshihiro Hiroshima University School of Dentistry, Professor, 歯学部, 教授 (00034182)
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| Co-Investigator(Kenkyū-buntansha) |
TSUJIMOTO Akira Hiroshima University School of Dentistry, Professor emeritus, 歯学部, 教授 (90034181)
MORITA Katsuya Hiroshima University School of Dentistry, Research Associate, 歯学部, 助手 (10116684)
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| Project Period (FY) |
1989 – 1990
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| Keywords | Platelet-activating factor / PAF / Catecholamine / Acetylcholine / Acetyltransferase / Calcium / Adrenal medulla |
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| Research Abstract |
Platelet-activating factor (PAF), originally detected in inflammatory and immunerelated cells, is a phospholipid mediator exhibiting a variety of biological activities, and thus physiological and pathological importances. Although PAF has been found in the neuronal tissue such as the brain, the role of PAF in the tissue is not known. We examined the production of PAF and its effects on catecholamine (CA) release in adrenal chromaffin cells. Acetylcholine (ACh) increased the amount of PAF in bovine adrenal chromaffin cells. The activity of lyso-PAF: acetyl-CoA acetyltransferase rapidly increased in the cells stimulated with ACh. PAF slightly increased CA release at high concentrations, and enhanced excess KCl-induced release of CA and the rise of intracelular free Ca^<2+> concentration ([Ca^<2+>]i). The effects of PAF on CA release and [Ca^<2+>]i were blocked by tetrodotoxin and partly reduced by calcium antagonists, but not inhibited by PAF antagonist, BN 52021. Low concentrations (1-100 nM) of PAF by itself had no effect on CA release but potentiated ACh-induced CA release in perfused adrenal glands. PAF also potentiated excess KCl-induced CA release but had little effect on caffeine-induced release in the absence of extracellular Ca^<2+>. Lyso-PAF was without effect. Low concentrations of PAF had no effect on [Ca^<2+>]i but potentiated ACh- and excess KCl-induced the increase in [Ca^<2+>]i. The effect of PAF was antagonized by BN 52021. The present results provide the evidence that PAF may play a modulating role in the CA release from adrenal chromaffin cells.
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