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Postsynaptic BDNF‐TrkB signaling in synapse maturation, plasticity, and disease
Author(s) -
Yoshii Akira,
ConstantinePaton Martha
Publication year - 2010
Publication title -
developmental neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.716
H-Index - 129
eISSN - 1932-846X
pISSN - 1932-8451
DOI - 10.1002/dneu.20765
Subject(s) - tropomyosin receptor kinase b , biology , neuroscience , synaptic plasticity , metaplasticity , brain derived neurotrophic factor , long term potentiation , postsynaptic potential , neurotrophic factors , microbiology and biotechnology , postsynaptic density , neurotrophin , synapse , receptor , genetics
Brain‐derived neurotrophic factor (BDNF) is a prototypic neurotrophin that regulates diverse developmental events from the selection of neural progenitors to the terminal dendritic differentiation and connectivity of neurons. We focus here on activity‐dependent synaptic regulation by BDNF and its receptor, full length TrkB. BDNF‐TrkB signaling is involved in transcription, translation, and trafficking of proteins during various phases of synaptic development and has been implicated in several forms of synaptic plasticity. These functions are carried out by a combination of the three signaling cascades triggered when BDNF binds TrkB: The mitogen‐activated protein kinase (MAPK), the phospholipase Cγ (PLC PLCγ), and the phosphatidylinositol 3‐kinase (PI3K) pathways. MAPK and PI3K play crucial roles in both translation and/or trafficking of proteins induced by synaptic activity, whereas PLCγ regulates intracellular Ca 2+ that can drive transcription via cyclic AMP and a protein kinase C. Conversely, the abnormal regulation of BDNF is implicated in various developmental and neurodegenerative diseases that perturb neural development and function. We will discuss the current state of understanding BDNF signaling in the context of synaptic development and plasticity with a focus on the postsynaptic cell and close with the evidence that basic mechanisms of BDNF function still need to be understood to effectively treat genetic disruptions of these pathways that cause devastating neurodevelopmental diseases. © 2010 Wiley Periodicals, Inc. Develop Neurobiol 2010