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Title: Postsynaptic Spiking Homeostatically Induces Cell-Autonomous Regulation of Inhibitory Inputs via Retrograde Signaling
Author: Peng, Yi-Rong ; Zeng, Si-Yu ; Song, He-Ling ; Li, Min-Yin ; Yamada, Maki K. ; Yu, Xiang
Source: JOURNAL OF NEUROSCIENCE
Issued Date: 2010
Volume: 30, Issue:48, Pages:16220-16231
Keyword: ACTIVITY-DEPENDENT REGULATION ; PRESYNAPTIC TRANSMITTER RELEASE ; CULTURED HIPPOCAMPAL-NEURONS ; NEUROTROPHIC FACTOR ; SYNAPTIC PLASTICITY ; FUNCTIONAL EXPRESSION ; GLUTAMATE RECEPTORS ; VESICULAR GLUTAMATE ; QUANTAL SIZE ; KAINIC ACID
Subject: Neurosciences & Neurology
Corresponding Author: Yu, XA (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Neurosci, Shanghai 200031, Peoples R China,yuxiang@ion.ac.cn
English Abstract: 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.
Indexed Type: sci
Language: 英语
Content Type: 期刊论文
URI: http://ir.sibs.ac.cn/handle/331001/1564
Appears in Collections:神经所(总)_期刊论文
树突发育与神经环路形成研究组_期刊论文

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Peng, Yi-Rong; Zeng, Si-Yu; Song, He-Ling; Li, Min-Yin; Yamada, Maki K.; Yu, Xiang.Postsynaptic Spiking Homeostatically Induces Cell-Autonomous Regulation of Inhibitory Inputs via Retrograde Signaling,JOURNAL OF NEUROSCIENCE,2010,30(48):16220-16231
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