Neurotrophin-3 mediates the autocrine survival of the catecholaminergic CAD CNS neuronal cell line.

摘要: The mechanisms for neuronal survival in the CNS are not well understood, but likely to be complex due possible autocrine and redundant neurotrophic support. Most studies have focused on nerve growth factor (NGF)/TrkA pathway peripheral neurons, little is known regarding other neurotrophins, particularly neurotrophin-3 (NT3)/TrkC. Progress has also been hampered by paucity of homogenous accessible experimental models. We now report that novel catecholaminergic cell line, CAD, capable mediated NT3. CAD origin can survive morphologically differentiate absence exogenously provided trophic factors. However, neutralizing reagents against NT3 (the TrkC-IgG fusion protein anti-NT3 antibodies), those block inhibited differentiating cells. Moreover, Trk phosphorylation was detected cells its inhibition K252a correlated with K252a-induced apoptosis. Finally, endogenous detectable extracts a specific ELISA assay. Thus, possess an capability NT3, may provide valuable model system studying signaling pathways mediate actions this understood neurotrophin.