Abstract:
:Brain-derived neurotrophic factor (BDNF) and its receptor, TrkB, are broadly expressed in the developing and adult mammalian brain. BDNF/TrkB-stimulated intracellular signaling is critical for neuronal survival, morphogenesis, and plasticity. It is well known that binding of BDNF to TrkB elicits various intracellular signaling pathways, including mitogen-activated protein kinase/extracellular signal-regulated protein kinase (MAPK/ERK), phospholipase Cg (PLCg), and phosphoinositide 3-kinase (PI3K) pathways, and that BDNF exerts biological effects on neurons via activation of similar mechanisms. In addition to TrkB, a low-affinity receptor p75 is also involved in neuronal survival and plasticity. BDNF affects neurons positively or negatively through various intracellular signaling pathways triggered by activation of TrkB or p75. From a clinical standpoint, roles of BDNF have been implicated in the pathophysiology of various brain diseases. The stress-induced steroid hormone, glucocorticoid, and BDNF are putatively associated with the pathophysiology of depression. Recent reports, including our studies, demonstrate possible crosstalk between glucocorticoid- and BDNF/TrkB-mediated signaling. Here, we present a broad overview of the current knowledge concerning BDNF action and associated intracellular signaling as it relates to neuronal protection, synaptic function, and morphological change. Furthermore, understanding the secretion and intracellular dynamics of BDNF proteins is critical as the fate of secreted BDNF may contribute to differences in neuronal response.
journal_name
Histol Histopatholjournal_title
Histology and histopathologyauthors
Numakawa T,Suzuki S,Kumamaru E,Adachi N,Richards M,Kunugi Hdoi
10.14670/HH-25.237subject
Has Abstractpub_date
2010-02-01 00:00:00pages
237-58issue
2eissn
0213-3911issn
1699-5848journal_volume
25pub_type
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