Department of Biomedicine, University of Bergen, Jonas Lies vei 91, 5009 Bergen, Norway; KG Jebsen Centre for Research on Neuropsychiatric Disorders, University of Bergen, Jonas Lies vei 91, 5009 Bergen, Norway.
Neuropharmacology. 2014 Jan;76 Pt C:664-76. doi: 10.1016/j.neuropharm.2013.06.024. Epub 2013 Jul 2.
Unraveling the molecular mechanisms governing long-term synaptic plasticity is a key to understanding how the brain stores information in neural circuits and adapts to a changing environment. Brain-derived neurotrophic factor (BDNF) has emerged as a regulator of stable, late phase long-term potentiation (L-LTP) at excitatory glutamatergic synapses in the adult brain. However, the mechanisms by which BDNF triggers L-LTP are controversial. Here, we distill and discuss the latest advances along three main lines: 1) TrkB receptor-coupled translational control underlying dendritic protein synthesis and L-LTP, 2) Mechanisms for BDNF-induced rescue of L-LTP when protein synthesis is blocked, and 3) BDNF-TrkB regulation of actin cytoskeletal dynamics in dendritic spines. Finally, we explore the inter-relationships between BDNF-regulated mechanisms, how these mechanisms contribute to different forms of L-LTP in the hippocampus and dentate gyrus, and outline outstanding issues for future research. This article is part of the Special Issue entitled 'BDNF Regulation of Synaptic Structure, Function, and Plasticity'.
阐明调控长时程突触可塑性的分子机制是理解大脑如何在神经网络中存储信息以及如何适应不断变化的环境的关键。脑源性神经营养因子（BDNF）已成为成年大脑中兴奋性谷氨酸能突触上稳定的晚期长时程增强（L-LTP）的调节因子。然而，BDNF 触发 L-LTP 的机制仍存在争议。在这里，我们沿着以下三个主要方面总结和讨论最新进展：1）TrkB 受体偶联的翻译控制，其涉及树突蛋白合成和 L-LTP，2）BDNF 诱导的蛋白质合成阻断时 L-LTP 的挽救机制，以及 3）BDNF-TrkB 对树突棘中肌动蛋白细胞骨架动态的调节。最后，我们探讨了 BDNF 调节机制之间的相互关系，这些机制如何有助于海马体和齿状回中不同形式的 L-LTP，并概述了未来研究的突出问题。本文是特刊“BDNF 对突触结构、功能和可塑性的调节”的一部分。
