Guizzetti Marina, Moore Nadia H, Giordano Gennaro, Costa Lucio G
Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, Washington 98105, USA.
J Biol Chem. 2008 Nov 14;283(46):31884-97. doi: 10.1074/jbc.M801316200. Epub 2008 Aug 28.
Astrocytes have been shown to release factors that have promoting or inhibiting effects on neuronal development. However, mechanisms controlling the release of such factors from astrocytes are not well established. Astrocytes express muscarinic receptors whose activation stimulates a robust intracellular signaling, although the role of these receptors in glial cells is not well understood. Acetylcholine and acetylcholine receptors are present in the brain before synaptogenesis occurs and are believed to be involved in neuronal maturation. The present study was undertaken to investigate whether stimulation of muscarinic receptors in astrocytes would modulate neurite outgrowth in hippocampal neurons. Rat hippocampal neurons, co-cultured with rat cortical astrocytes previously exposed to the cholinergic agonist carbachol, displayed longer neurites. The effect of carbachol in astrocytes was due to the activation of M3 muscarinic receptors. Exposure of astrocytes to carbachol increased the expression of the extracellular matrix proteins fibronectin and laminin-1 in these cells. This effect was mediated in part by an increase in laminin-1 and fibronectin mRNA levels and in part by the up-regulation of the production and release of plasminogen activator inhibitor-1, an inhibitor of the proteolytic degradation of the extracellular matrix. The inhibition of fibronectin activity strongly reduced the effect of carbachol on the elongation of all the neurites, whereas inhibition of laminin-1 activity reduced the elongation of minor neurites only. Plasminogen activator inhibitor-1 also induced neurite elongation through a direct effect on neurons. Taken together, these results demonstrate that cholinergic muscarinic stimulation of astrocytes induces the release of permissive factors that accelerate neuronal development.
星形胶质细胞已被证明能释放对神经元发育具有促进或抑制作用的因子。然而,控制这些因子从星形胶质细胞释放的机制尚未完全明确。星形胶质细胞表达毒蕈碱受体,其激活可刺激强大的细胞内信号传导,尽管这些受体在神经胶质细胞中的作用尚不清楚。乙酰胆碱和乙酰胆碱受体在突触发生之前就存在于大脑中,并且被认为参与神经元成熟。本研究旨在探讨星形胶质细胞中毒蕈碱受体的刺激是否会调节海马神经元的神经突生长。与先前暴露于胆碱能激动剂卡巴胆碱的大鼠皮质星形胶质细胞共培养的大鼠海马神经元,其神经突更长。卡巴胆碱对星形胶质细胞的作用是由于M3毒蕈碱受体的激活。将星形胶质细胞暴露于卡巴胆碱会增加这些细胞中细胞外基质蛋白纤连蛋白和层粘连蛋白-1的表达。这种作用部分是由层粘连蛋白-1和纤连蛋白mRNA水平的增加介导的,部分是由纤溶酶原激活物抑制剂-1(一种细胞外基质蛋白水解降解的抑制剂)的产生和释放上调介导的。抑制纤连蛋白活性强烈降低了卡巴胆碱对所有神经突伸长的作用,而抑制层粘连蛋白-1活性仅降低了小神经突的伸长。纤溶酶原激活物抑制剂-1也通过对神经元的直接作用诱导神经突伸长。综上所述,这些结果表明星形胶质细胞的胆碱能毒蕈碱刺激诱导了促进神经元发育的允许因子的释放。