The sensitivity of the nervous system to receive and respond to events, both internal and in the environment, depends on the ability of neural structures to remodel in response to experience (Kandel 2001; Mayford et al. 2012)⁠. Neural plasticity depends on rapid, tightly controlled rearrangements of cytoskeleton, membrane morphology, and protein content. Neurons regulate plasticity across orders of structural organization, from changes in molecular machinery that calls forth the synaptic alterations that underlie learning and memory, to events that evoke mesoscale alterations in neurite architecture, and to the birth and death of neurons. We address the concept that the events responsible for such diverse modification of neurons originate from local changes in signaling and that understanding the underlying mechanisms requires an appreciation of the nature of constraints placed upon spatial and temporal activity. During development and in the adult, both the remodeling of specific subcellular structures and induction of synaptic plasticity require local control and regulation of signaling, including those initiated by activation of surface receptors (Reichardt 2006). As an example, the receptor tyrosine kinase TrkB, activated by its ligand brain-derived neurotrophic factor (BDNF), has emerged as a potent modulator of plasticity in both development and adulthood, from neurite pruning and branching events during PNS and CNS development, to learning and memory. Here, we review the mechanisms by which TrkB signaling engages in local remodeling to support neural plasticity.

中文翻译：

---

局部 TrkB 信号：发育和神经可塑性的主题

神经系统接收和响应内部和环境事件的敏感性取决于神经结构根据经验进行重塑的能力（Kandel 2001；Mayford 等人，2012）⁠。神经可塑性取决于细胞骨架、膜形态和蛋白质含量的快速、严格控制的重排。神经元调节跨结构组织顺序的可塑性，从引发学习和记忆基础的突触改变的分子机制的变化，到引起神经突结构中尺度改变的事件，再到神经元的诞生和死亡。我们提出了一个概念，即导致神经元的这种不同修饰的事件源于信号的局部变化，并且理解潜在机制需要了解对空间和时间活动施加的约束的性质。在发育过程中和在成人中，特定亚细胞结构的重塑和突触可塑性的诱导都需要对信号进行局部控制和调节，包括那些由表面受体激活引发的信号（Reichardt 2006）。例如，受体酪氨酸激酶 TrkB 被其配体脑源性神经营养因子 (BDNF) 激活，已成为发育和成年期可塑性的有效调节剂，从 PNS 和 CNS 发育期间的神经突修剪和分支事件，到学习和记忆。这里，