Neurotrophin signaling via receptor tyrosine kinases is essential for the development and function of the nervous system in vertebrates. TrkB activation and signaling show substantial differences to other receptor tyrosine kinases of the Trk family that mediate the responses to nerve growth factor and neurotrophin-3. Growing evidence suggests that TrkB cell surface expression is highly regulated and determines the sensitivity of neurons to brain-derived neurotrophic factor (BDNF). This translocation of TrkB depends on co-factors and modulators of cAMP levels, N-glycosylation, and receptor transactivation. This process can occur in very short time periods and the resulting rapid modulation of target cell sensitivity to BDNF could represent a mechanism for fine-tuning of synaptic plasticity and communication in complex neuronal networks. This review focuses on those modulatory mechanisms in neurons that regulate responsiveness to BDNF via control of TrkB surface expression.

中文翻译：

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TrkB 细胞表面表达的调节——一种调节神经元对脑源性神经营养因子反应的机制

通过受体酪氨酸激酶传递神经营养因子信号对于脊椎动物神经系统的发育和功能至关重要。TrkB 激活和信号传导显示与 Trk 家族的其他受体酪氨酸激酶存在显着差异，后者介导对神经生长因子和神经营养因子-3 的反应。越来越多的证据表明，TrkB 细胞表面表达受到高度调节，并决定了神经元对脑源性神经营养因子 (BDNF) 的敏感性。TrkB 的这种易位取决于 cAMP 水平、N-糖基化和受体反式激活的辅助因子和调节剂。这个过程可以在很短的时间内发生，由此产生的靶细胞对 BDNF 敏感性的快速调节可能代表了一种微调复杂神经元网络中突触可塑性和通信的机制。