cAMP potentiates β-amyloid-induced nitric oxide release from microglia

被引：12

作者：

Pyo, H ^{[1
]}

Jou, I ^{[1
]}

Jung, S ^{[1
]}

Joe, E ^{[1
]}

机构：

[1] Ajou Univ, Sch Med, Dept Pharmacol, Paldal Gu, Suwon 442749, Kyunggi Do, South Korea

来源：

NEUROREPORT | 1999年 / 10卷 / 01期

关键词：

beta-amyloid peptide; cAMP; microglia; nitric oxide;

D O I：

10.1097/00001756-199901180-00007

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

THE beta-amyloid peptide (A beta) has been known to activate microglia and to induce release of nitric oxide (NO). In this study, we examined the effect of cAMP on A beta-induced microglial activation using cultured rat brain microglia. Dibutyryl-cAMP (dbcAMP) and 3-isobutyl-1-methylxanthine (IBMX) significantly potentiated A beta(25-35)- or A beta(1-42)-induced NO release in a dose-dependent manner. The increase in NO release was due to the increased expression of inducible nitric oxide synthase (iNOS). However, forskolin, an adenylate cyclase activator, weakly increased NO release at 10-50 mu M but caused a decrease at 100 mu M. These results suggest that increase in intracellular cAMP could potentiate microglial activation induced by A beta. (C) 1999 Lippincott Williams & Wilkins.

引用

页码：37 / 40

页数：4

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