CaMKII Autophosphorylation Is Necessary for Optimal Integration of Ca(2+) Signals during LTP Induction, but Not Maintenance.
CaMKII Autophosphorylation Is Necessary for Optimal Integration of Ca(2+) Signals during LTP Induction, but Not Maintenance.
复制标题
CAMKII自磷酸化对于在LTP诱导期间的CA（2+）信号的最佳整合是必需的，但不是维护。
DOI：
10.1016/j.neuron.2017.04.041
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发表时间：
2017-05-17
期刊：
影响因子：
16.2
通讯作者：
Yasuda R
中科院分区：
文献类型：
--
作者：
Chang JY;Parra-Bueno P;Laviv T;Szatmari EM;Lee SR;Yasuda R
CaMKII在解码钙（Ca2+）信号以启动持久的突触可塑性中起关键作用。然而，CaMKII介导的Ca2+信号在脊柱的属性仍然难以捉摸。在这里，我们使用快速成帧双光子荧光寿命成像测量了脊椎中的CaMKII活性。在重复的Ca2+升高过程中，每个脉冲后，CaMKII活性以逐步的方式增加。Thr286磷酸化减慢了CaMKII的衰变，从而降低了诱导脊柱可塑性所需的频率。在Thr 286磷酸化不存在的情况下，增加刺激频率导致足以诱导可塑性的高峰突变体CaMKIIT 286 A活性。我们的研究结果表明，Thr286磷酸化通过整合Ca 2+信号在诱导LTP中起着重要作用，它极大地促进了CaMK II和LTP的激活，但对CaMK II和LTP的激活是不利的。
CaMKII plays a critical role in decoding calcium (Ca2+) signals to initiate long-lasting synaptic plasticity. However, the properties of CaMKII that mediate Ca2+ signals in spines remain elusive. Here, we measured CaMKII activity in spines using fast-framing two-photon fluorescence lifetime imaging. Following each pulse during repetitive Ca2+ elevations, CaMKII activity increased in a stepwise manner. Thr286 phosphorylation slows the decay of CaMKII and thus, lowers the frequency required to induce spine plasticity by several fold. In the absence of Thr286 phosphorylation, increasing the stimulation frequency results in high peak mutant CaMKIIT286A activity that is sufficient for inducing plasticity. Our findings demonstrate that Thr286 phosphorylation plays an important role in induction of LTP by integrating Ca2+ signals, and it greatly promotes, but is dispensable for the activation of CaMKII and LTP.
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影响因子：
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作者：
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通讯作者：
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