Activation of CaMKII in single dendritic spines during long-term potentiation.

Activation of CaMKII in single dendritic spines during long-term potentiation.
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DOI:
10.1038/nature07842
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发表时间:
2009-03-19
期刊:
影响因子:
64.8
通讯作者:
Yasuda, Ryohei
Yasuda, Ryohei
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Lee, Seok-Jin R.;Escobedo-Lozoya, Yasmin;Szatmari, Erzsebet M.;Yasuda, Ryohei

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Ca 2 + /钙调蛋白依赖性激酶II(CaMKII)在长时程增强(LTP)中起着重要作用,LTP是某些形式的学习和记忆的基础。在这里,我们监测的时空动态的CaMKII激活在个别树突棘在LTP使用2-光子荧光寿命成像显微镜结合2-光子谷氨酸释放。诱导LTP和相关的脊柱扩大在单一的脊椎触发短暂的(101分钟)CaMKII激活限于刺激的脊柱。脊髓中的CaMKII被NMDA受体和L型电压敏感性钙通道特异性激活,推测是通过通道附近的纳米结构域Ca 2+,分别响应于谷氨酸释放和去极化。高度的区室化和通道特异性的CaMKII信号允许刺激特异性的时空模式的CaMKII信号,可能是重要的突触特异性的突触可塑性。
Ca2+ / Calmodulin-dependent kinase II (CaMKII) plays a central role in long-term potentiation (LTP), which underlies some forms of learning and memory. Here we monitored the spatiotemporal dynamics of CaMKII activation in individual dendritic spines during LTP using 2-photon fluorescence lifetime imaging microscopy in combination with 2-photon glutamate uncaging. Induction of LTP and associated spine enlargement in single spines triggered transient (∼ 1 min) CaMKII activation restricted to the stimulated spines. CaMKII in spines was specifically activated by NMDA receptors and L-type voltage sensitive calcium channels, presumably via nanodomain Ca2+ near the channels, in response to glutamate uncaging and depolarization, respectively. The high degree of compartmentalization and channel specificity of CaMKII signalling allow stimuli-specific spatiotemporal patterns of CaMKII signalling and may be important for synapse-specificity of synaptic plasticity.
CAMKII将Ca2+通道的camkii tethers建立,建立了Ca2+信号的本地和专用集成商进行便利。
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