Arc-dependent synapse-specific homeostatic plasticity

被引:136
作者
Beique, Jean-Claude [1 ,2 ]
Na, Youn [1 ,2 ]
Kuhl, Dietmar [3 ]
Worley, Paul F. [1 ]
Huganir, Richard L. [1 ,2 ]
机构
[1] Univ Med Ctr Hamburg Eppendorf, Solomon Snyder Dept Neurosci, D-20246 Hamburg, Germany
[2] Univ Med Ctr Hamburg Eppendorf, Howard Hughes Med Inst, D-20246 Hamburg, Germany
[3] Univ Med Ctr Hamburg Eppendorf, Ctr Mol Neurobiol, D-20246 Hamburg, Germany
基金
美国国家卫生研究院;
关键词
AMPA receptors; GluA2-lacking receptors; spines; LONG-TERM POTENTIATION; GLUR2-LACKING AMPA RECEPTORS; DENDRITIC SPINES; HIPPOCAMPAL SYNAPSES; SUBUNIT COMPOSITION; PYRAMIDAL NEURONS; EXPRESSION; TRAFFICKING; DEPRESSION; ARC/ARG3.1;
D O I
10.1073/pnas.1017914108
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Both theoretical and experimental research has indicated that the synaptic strength between neurons in a network needs to be properly fine-tuned and controlled by homeostatic mechanisms to ensure proper network function. One such mechanism that has been extensively characterized is synaptic homeostatic plasticity or global synaptic scaling. This mechanism refers to the bidirectional ability of all synapses impinging on a neuron to actively compensate for changes in the neuron's overall excitability. Here, using a combination of electrophysiological, two-photon glutamate uncaging and imaging methods, we show that mature individual synapses, independent of neighboring synapses, have the ability to autonomously sense their level of activity and actively compensate for it in a homeostatic-like fashion. This synapse-specific homeostatic plasticity, similar to global synaptic plasticity, requires the immediate early gene Arc. Together, our results document an extra level of regulation of synaptic function that bears important computational consequences on information storage in the brain.
引用
收藏
页码:816 / 821
页数:6
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