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Studies on the neural functions of platelet-activating factor

血小板活化因子的神经功能研究

基本信息

批准号：
01571019
负责人：
DOHI Toshihiro
金额：
$ 1.34万
依托单位：
HIROSHIMA UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1989
资助国家：
日本
起止时间：
1989 至 1990
项目状态：
已结题

项目摘要

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.

血小板活化因子（PAF）最初在炎症和免疫相关细胞中检测到，是一种磷脂介质，具有多种生物活性，因此具有生理和病理重要性。虽然在大脑等神经组织中发现了PAF，但PAF在组织中的作用尚不清楚。我们研究了PAF的产生及其对肾上腺染色质细胞中儿茶酚胺（CA）释放的影响。乙酰胆碱（ACh）增加了牛肾上腺嗜铬细胞中PAF的含量。乙酰辅酶a乙酰转移酶活性在乙酰胆碱刺激下迅速升高。PAF在高浓度下略微增加CA的释放，并增强过量kcl诱导的CA释放和细胞内游离CA ^<2+>浓度的升高（[CA ^<2+>]i）。PAF对CA释放和[CA ^<2+>]i的影响被河豚毒素阻断，钙拮抗剂部分降低，但PAF拮抗剂BN 52021不抑制。低浓度（1-100 nM） PAF本身对CA释放没有影响，但会增强乙酰胆碱诱导的灌注肾上腺CA释放。PAF也增强了过量的kcl诱导的CA释放，但在细胞外CA ^<2+>缺乏的情况下，对咖啡因诱导的CA释放影响不大。Lyso-PAF没有效果。低浓度PAF对[Ca^<2+>]i没有影响，但增强了ACh-，过量的kcl诱导了[Ca^<2+>]i的增加。BN 52021可拮抗PAF的作用。本研究结果表明，PAF可能在肾上腺染色质细胞CA释放中起调节作用。