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Title: Brain-derived neurotrophic factor-tropomyosin-related kinase B signaling contributes to activity-dependent changes in synaptic proteins
Author: Jia, Jie-Min ; Chen, Qian ; Zhou, Yang ; Miao, Sheng ; Zheng, Jing ; Zhang, Chi ; null(熊志奇)
Source: JOURNAL OF BIOLOGICAL CHEMISTRY
Issued Date: 2008
Volume: 283, Issue:30, Pages:21242-21250
Keyword: UBIQUITIN-PROTEASOME SYSTEM ; MESSENGER-RNA ; HIPPOCAMPAL-NEURONS ; DEGRADATION ; BDNF ; CREB ; MODULATION ; EXPRESSION ; PLASTICITY ; RECEPTORS
Subject: Biochemistry & Molecular Biology
Corresponding Author: Xiong, ZQ (reprint author), Chinese Acad Sci, Inst Neurosci, Shanghai Inst Biol Sci, 320 Yueyang Rd, Shanghai 200031, Peoples R China,xiongzhiqi@ion.ac.cn
English Abstract: The ability of synapses to undergo changes in structure and function in response to alterations of neuronal activity is an essential property of neural circuits. One way that this is achieved is through global changes in the molecular composition of the synapse; however, it is not clear how these changes are coupled to the dynamics of neuronal activity. Here we found that, in cultured rat cortical neurons, bidirectional changes of neuronal activity led to corresponding alterations in the expression of brain-derived neurotrophic factor (BDNF) and phosphorylation of its receptor tropomyosin-related kinase B (TrkB), as well as in the level of synaptic proteins. Exogenous BDNF reversed changes in synaptic proteins induced by chronic activity blockade, while inhibiting Trk kinase activity or depleting endogenous BDNF abolished the concentration changes induced by chronic activity elevation. Both tetrodotoxin and bicuculline had significant, but opposite, effects on synaptic protein ubiquitination in a time-dependent manner. Furthermore, exogenous BDNF was sufficient to increase ubiquitination of synaptic proteins, whereas scavenging endogenous BDNF or inhibiting Trk kinase activity prevented the ubiquitination of synaptic proteins induced by chronic elevation of neuronal activity. Inhibiting the proteasome or blocking protein polyubiquitination mimicked the effect of tetrodotoxin on the levels of synaptic proteins and canceled the effects of BDNF. Our study indicates that BDNF-TrkB signaling acts upstream of the ubiquitin proteasome system, linking neuronal activity to protein turnover at the synapse.
Indexed Type: sci
Language: 英语
Content Type: 期刊论文
URI: http://ir.sibs.ac.cn/handle/331001/1710
Appears in Collections:神经所(总)_期刊论文
疾病神经生物学研究组_期刊论文

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Jia, Jie-Min; Chen, Qian; Zhou, Yang; Miao, Sheng; Zheng, Jing; Zhang, Chi; Xiong, Zhi-Qi.Brain-derived neurotrophic factor-tropomyosin-related kinase B signaling contributes to activity-dependent changes in synaptic proteins,JOURNAL OF BIOLOGICAL CHEMISTRY,2008,283(30):21242-21250
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