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受体酪氨酸激酶B介导的兴奋性突触形成。

Receptor tyrosine kinase B-mediated excitatory synaptogenesis.

作者信息

Luikart Bryan W, Parada Luis F

机构信息

Center for Developmental Biology, and Kent Waldrep Foundation Center for Basic Neuroscience Research on Nerve Growth and Regeneration, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.

出版信息

Prog Brain Res. 2006;157:15-24. doi: 10.1016/s0079-6123(06)57002-5.

Abstract

The receptor tyrosine kinase B, TrkB, is the high-affinity receptor for brain-derived neurotrophic factor (BDNF). Much evidence supports a role for TrkB signaling in excitatory synapse formation. There have been a number of recent advances in understanding the cell biology of TrkB-mediated excitatory synaptogenesis. The predominant mechanism by which TrkB supports excitatory synaptogenesis appears to be due to cell-autonomous signaling in both pre- and postsynaptic cells. This signaling appears to contribute to the growth and stabilization processes necessary for the net formation of synapses during development. Further, the molecular mechanisms by which TrkB contributes to these growth and stabilization processes are beginning to be elucidated.

摘要

受体酪氨酸激酶B(TrkB)是脑源性神经营养因子(BDNF)的高亲和力受体。大量证据支持TrkB信号传导在兴奋性突触形成中发挥作用。在理解TrkB介导的兴奋性突触发生的细胞生物学方面,最近有了许多进展。TrkB支持兴奋性突触发生的主要机制似乎是由于突触前和突触后细胞中的细胞自主信号传导。这种信号传导似乎有助于发育过程中突触净形成所需的生长和稳定过程。此外,TrkB促成这些生长和稳定过程的分子机制也开始得到阐明。

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