Brain-derived neurotrophic factor-tropomyosin-related kinase B signaling contributes to activity-dependent changes in synaptic proteins
文献类型：期刊论文
| 作者 | Xiong, Zhi-Qi
|
| 刊名 | JOURNAL OF BIOLOGICAL CHEMISTRY
 |
| 出版日期 | 2008 |
| 卷号 | 283期号:30页码:21242-21250 |
| 关键词 | UBIQUITIN-PROTEASOME SYSTEM MESSENGER-RNA HIPPOCAMPAL-NEURONS DEGRADATION BDNF CREB MODULATION EXPRESSION PLASTICITY RECEPTORS |
| ISSN号 | 0021-9258 |
| 通讯作者 | 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 |
| 英文摘要 | 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. |
| 学科主题 | Biochemistry & Molecular Biology |
| 收录类别 | SCI |
| 语种 | 英语 |
| 公开日期 | 2012-07-23 |
| 源URL | [http://ir.sibs.ac.cn/handle/331001/1710]  |
| 专题 | 上海神经科学研究所_神经所(总) 上海神经科学研究所_疾病神经生物学研究组 |
| 推荐引用方式 GB/T 7714 | Xiong, Zhi-Qi. Brain-derived neurotrophic factor-tropomyosin-related kinase B signaling contributes to activity-dependent changes in synaptic proteins[J]. JOURNAL OF BIOLOGICAL CHEMISTRY,2008,283(30):21242-21250. |
| APA | Xiong, Zhi-Qi.(2008).Brain-derived neurotrophic factor-tropomyosin-related kinase B signaling contributes to activity-dependent changes in synaptic proteins.JOURNAL OF BIOLOGICAL CHEMISTRY,283(30),21242-21250. |
| MLA | Xiong, Zhi-Qi."Brain-derived neurotrophic factor-tropomyosin-related kinase B signaling contributes to activity-dependent changes in synaptic proteins".JOURNAL OF BIOLOGICAL CHEMISTRY 283.30(2008):21242-21250. |
入库方式： OAI收割
来源：上海神经科学研究所
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