Canossa M, Griesbeck O, Berninger B, Campana G, Kolbeck R, Thoenen H
Department of Neurobiochemistry, Max Planck Institute for Psychiatry, Martinsried, Germany.
Proc Natl Acad Sci U S A. 1997 Nov 25;94(24):13279-86. doi: 10.1073/pnas.94.24.13279.
Neurotrophins, secreted in an activity-dependent manner, are thought to be involved in the activity-dependent refinement of synaptic connections. Here we demonstrate that in hippocampal neurons and the rat pheochromocytoma cell line PC12 application of exogenous neurotrophins induces secretion of neurotrophins, an effect that is mediated by the activation of tyrosine kinase neurotrophin receptors (Trks). Like activity-dependent secretion of neurotrophins, neurotrophin-induced neurotrophin secretion requires mobilization of calcium from intracellular stores. Because neurotrophins are likely to be released from both dendrites and axons, neurotrophin-induced neurotrophin release represents a potential positive feedback mechanism, contributing to the reinforcement and stabilization of synaptic connections.
神经营养因子以活动依赖的方式分泌,被认为参与了突触连接的活动依赖型精细化过程。在此我们证明,在海马神经元和大鼠嗜铬细胞瘤细胞系PC12中,外源性神经营养因子的应用会诱导神经营养因子的分泌,这一效应由酪氨酸激酶神经营养因子受体(Trks)的激活介导。与神经营养因子的活动依赖型分泌一样,神经营养因子诱导的神经营养因子分泌需要从细胞内储存库动员钙。由于神经营养因子可能从树突和轴突两者释放出来,神经营养因子诱导的神经营养因子释放代表了一种潜在的正反馈机制,有助于突触连接的强化和稳定。