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脂多糖诱导培养的小脑颗粒神经元中的一氧化氮合酶活性。

Lipopolysaccharide-induced nitric oxide synthase activity in cultured cerebellar granule neurons.

作者信息

Sato I, Himi T, Murota S

机构信息

Department of Physiological Chemistry, Graduate School, Tokyo Medical and Dental University, Japan.

出版信息

Neurosci Lett. 1996 Feb 16;205(1):45-8. doi: 10.1016/0304-3940(96)12377-6.

DOI:10.1016/0304-3940(96)12377-6
PMID:8867017
Abstract

We examined the inducible form of nitric oxide synthase (iNOS) activity in cerebellar primary cultures enriched with granule neurons. Treatment with lipopolysaccharide (LPS) for 24 h was performed in two different cultures in which the survival of neurons was controlled by the levels of extracellular K+. Treatment of the granule neurons with the contaminating non-neuronal cells (< 5%) in a high K+ (25 mM) -containing culture medium with LPS induced four-fold NOS activity compared to that of the control, and the induced NOS activity was calcium-independent. LPS did not induce the NOS activity at all in the contaminating non-neuronal cells alone which were obtained by eliminating all the granule neurons from the culture by lowering the K+ concentration (5 mM). We conclude that the LPS-activated granule neurons can express iNOS activity and that this induction is not attributable to the contaminating nonneuronal cells.

摘要

我们检测了富含颗粒神经元的小脑原代培养物中一氧化氮合酶(iNOS)的诱导型活性。在两种不同的培养物中用脂多糖(LPS)处理24小时,其中神经元的存活由细胞外K +水平控制。在含有高K +(25 mM)的培养基中用污染的非神经元细胞(<5%)处理颗粒神经元并加入LPS,与对照相比,诱导的NOS活性增加了四倍,并且诱导的NOS活性不依赖于钙。单独在通过降低K +浓度(5 mM)从培养物中消除所有颗粒神经元而获得的污染非神经元细胞中,LPS根本不诱导NOS活性。我们得出结论,LPS激活的颗粒神经元可以表达iNOS活性,并且这种诱导不归因于污染的非神经元细胞。

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