TrkB (neuronal receptor tyrosine kinase-2, NTRK2) is the receptor for brain-derived neurotrophic factor (BDNF) and is a critical regulator of activity-dependent neuronal plasticity. The past few years have witnessed an increasing understanding of the structure and function of TrkB, including its transmembrane domain (TMD). TrkB interacts with membrane cholesterol, which bidirectionally regulates TrkB signaling. Additionally, TrkB has recently been recognized as a binding target of antidepressant drugs. A variety of different antidepressants, including typical and rapid-acting antidepressants, as well as psychedelic compounds, act as allosteric potentiators of BDNF signaling through TrkB. This suggests that TrkB is the common target of different antidepressant compounds. Although more research is needed, current knowledge suggests that TrkB is a promising target for further drug development.

中文翻译：

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TrkB 跨膜结构域：将结构理解与治疗策略联系起来

TrkB（神经元受体酪氨酸激酶-2，NTRK2）是脑源性神经营养因子 (BDNF) 的受体，是活动依赖性神经元可塑性的关键调节因子。在过去的几年里，人们对 TrkB 的结构和功能，包括其跨膜结构域 (TMD) 的了解不断加深。 TrkB 与膜胆固醇相互作用，双向调节 TrkB 信号传导。此外，TrkB 最近被认为是抗抑郁药物的结合靶点。多种不同的抗抑郁药，包括典型的速效抗抑郁药以及迷幻化合物，可通过 TrkB 作为 BDNF 信号传导的变构增强剂。这表明 TrkB 是不同抗抑郁化合物的共同靶点。尽管还需要更多的研究，但目前的知识表明 TrkB 是进一步药物开发的一个有希望的目标。