Postsynaptic Spiking Homeostatically Induces Cell-Autonomous Regulation of Inhibitory Inputs via Retrograde Signaling
文献类型：期刊论文
| 作者 | Peng, Yi-Rong ; Zeng, Si-Yu ; Song, He-Ling ; Li, Min-Yin ; Yamada, Maki K. ; Yu, Xiang |
| 刊名 | JOURNAL OF NEUROSCIENCE
 |
| 出版日期 | 2010 |
| 卷号 | 30期号:48页码:16220-16231 |
| ISSN号 | 0270-6474 |
| 关键词 | ACTIVITY-DEPENDENT REGULATION PRESYNAPTIC TRANSMITTER RELEASE CULTURED HIPPOCAMPAL-NEURONS NEUROTROPHIC FACTOR SYNAPTIC PLASTICITY FUNCTIONAL EXPRESSION GLUTAMATE RECEPTORS VESICULAR GLUTAMATE QUANTAL SIZE KAINIC ACID |
| 通讯作者 | Yu, XA (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Neurosci, Shanghai 200031, Peoples R China,yuxiang@ion.ac.cn |
| 英文摘要 | Developing neural circuits face the dual challenge of growing in an activity-induced fashion and maintaining stability through homeostatic mechanisms. Compared to our understanding of homeostatic regulation of excitatory synapses, relatively little is known about the mechanism mediating homeostatic plasticity of inhibitory synapses, especially that following activity elevation. Here, we found that elevating neuronal activity in cultured hippocampal neurons for 4 h significantly increased the frequency and amplitude of mIPSCs, before detectable change at excitatory synapses. Consistently, we observed increases in presynaptic and postsynaptic proteins of GABAergic synapses, including GAD65, vGAT, and GABA(A)R alpha 1. By suppressing activity-induced increase of neuronal firing with expression of the inward rectifier potassium channel Kir2.1 in individual neurons, we showed that elevation in postsynaptic spiking activity is required for activity-dependent increase in the frequency and amplitude of mIPSCs. Importantly, directly elevating spiking in individual postsynaptic neurons, by capsaicin activation of overexpressed TRPV1 channels, was sufficient to induce increased mIPSCamplitude and frequency, mimicking the effect of elevated neuronal activity. Downregulating BDNF expression in the postsynaptic neuron or its extracellular scavenging prevented activity-induced increase in mIPSC frequency, consistent with a role of BDNF-dependent retrograde signaling in this process. Finally, elevating activity in vivo by kainate injection increased both mIPSC amplitude and frequency in CA1 pyramidal neurons. Thus, spiking-induced, cell-autonomous upregulation of GABAergic synaptic inputs, through retrograde BDNF signaling, represents an early adaptive response of neural circuits to elevated network activity. |
| 学科主题 | Neurosciences & Neurology |
| 资助信息 | Ministry of Science and Technology[2006CB806600, 2006CB943903]; National Natural Science Foundation of China[30721004]; Chinese Academy of Sciences[KSCX2-YW-R-103] |
| 收录类别 | SCI |
| 语种 | 英语 |
| 公开日期 | 2012-07-13 |
| 源URL | [http://ir.sibs.ac.cn/handle/331001/1564]  |
| 专题 | 上海神经科学研究所_神经所(总) 上海神经科学研究所_树突发育与神经环路形成研究组 |
| 推荐引用方式 GB/T 7714 | Peng, Yi-Rong,Zeng, Si-Yu,Song, He-Ling,et al. Postsynaptic Spiking Homeostatically Induces Cell-Autonomous Regulation of Inhibitory Inputs via Retrograde Signaling[J]. JOURNAL OF NEUROSCIENCE,2010,30(48):16220-16231. |
| APA | Peng, Yi-Rong,Zeng, Si-Yu,Song, He-Ling,Li, Min-Yin,Yamada, Maki K.,&Yu, Xiang.(2010).Postsynaptic Spiking Homeostatically Induces Cell-Autonomous Regulation of Inhibitory Inputs via Retrograde Signaling.JOURNAL OF NEUROSCIENCE,30(48),16220-16231. |
| MLA | Peng, Yi-Rong,et al."Postsynaptic Spiking Homeostatically Induces Cell-Autonomous Regulation of Inhibitory Inputs via Retrograde Signaling".JOURNAL OF NEUROSCIENCE 30.48(2010):16220-16231. |
入库方式： OAI收割
来源：上海神经科学研究所
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