Sasi Manju, Vignoli Beatrice, Canossa Marco, Blum Robert
Institute of Clinical Neurobiology, University Hospital, University of Würzburg, 97078, Würzburg, Germany.
Centre for Integrative Biology (CIBIO), University of Trento, 38123, Povo, TN, Italy.
Pflugers Arch. 2017 Jun;469(5-6):593-610. doi: 10.1007/s00424-017-1964-4. Epub 2017 Mar 9.
Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family of secreted proteins. Signaling cascades induced by BDNF and its receptor, the receptor tyrosine kinase TrkB, link neuronal growth and differentiation with synaptic plasticity. For this reason, interference with BDNF signaling has emerged as a promising strategy for potential treatments in psychiatric and neurological disorders. In many brain circuits, synaptically released BDNF is essential for structural and functional long-term potentiation, two prototypical cellular models of learning and memory formation. Recent studies have revealed an unexpected complexity in the synaptic communication of mature BDNF and its precursor proBDNF, not only between local pre- and postsynaptic neuronal targets but also with participation of glial cells. Here, we consider recent findings on local actions of the BDNF family of ligands at the synapse and discuss converging lines of evidence which emerge from per se conflicting results.
脑源性神经营养因子（BDNF）是分泌蛋白神经营养因子家族的一员。BDNF及其受体——受体酪氨酸激酶TrkB所诱导的信号级联反应，将神经元的生长和分化与突触可塑性联系起来。因此，干扰BDNF信号传导已成为治疗精神疾病和神经疾病的一种有前景的策略。在许多脑回路中，突触释放的BDNF对于结构和功能的长期增强至关重要，这是学习和记忆形成的两种典型细胞模型。最近的研究揭示了成熟BDNF及其前体proBDNF在突触通讯中的意外复杂性，不仅存在于局部突触前和突触后神经元靶点之间，而且还有胶质细胞的参与。在这里，我们考虑BDNF配体家族在突触处的局部作用的最新发现，并讨论从本身相互矛盾的结果中得出的一致证据。
