Department of Animal and Human Biology, University of Torino, Torino, Italy.
J Neurosci Res. 2009 Oct;87(13):2951-62. doi: 10.1002/jnr.22116.
Basic fibroblast growth factor (bFGF) exerts multiple neurotrophic actions on cultured neurons from the ciliary ganglion of chick embryo, among them promotion of neuronal survival and of neurite outgrowth. To understand the specificity of the signal transduction cascades involved in the control of these processes, we used pharmacological inhibitors of the three main effectors known to act downstream of the bFGF receptor (FGFR): phospholipase Cgamma (PLCgamma), mitogen-activated protein kinase (MAPK), and phosphatidylinositol 3-kinase (PI3-K). Neuronal survival was assessed at 24 and 48 hr; neurite growth was analyzed both on dissociated neurons and on explants of whole ganglia. Our data show that only the PI3-K pathway is involved in the survival-promoting effect of bFGF; on the other hand, all three effectors converge on the enhancement of neurite outgrowth, both on isolated neurons and in whole ganglia.
碱性成纤维细胞生长因子（bFGF）对鸡胚睫状神经节培养的神经元具有多种神经营养作用，其中包括促进神经元存活和突起生长。为了了解参与控制这些过程的信号转导级联的特异性，我们使用了三种已知作用于碱性成纤维细胞生长因子受体（FGFR）下游的主要效应物的药理学抑制剂：磷脂酶 Cγ（PLCγ）、丝裂原活化蛋白激酶（MAPK）和磷酸肌醇 3-激酶（PI3-K）。在 24 和 48 小时评估神经元存活；在分离的神经元和整个神经节的外植体上分析突起生长。我们的数据表明，只有 PI3-K 途径参与了 bFGF 促进存活的作用；另一方面，所有三种效应物都集中在增强突起生长上，无论是在分离的神经元上还是在整个神经节上。
