钙/钙调蛋白依赖性蛋白激酶II（CaMKII）自身磷酸化对于长时程增强（LTP）诱导过程中钙信号的最佳整合是必要的，但对于LTP维持并非必要。
CaMKII Autophosphorylation Is Necessary for Optimal Integration of Ca Signals during LTP Induction, but Not Maintenance.
作者信息
Chang Jui-Yun, Parra-Bueno Paula, Laviv Tal, Szatmari Erzsebet M, Lee Seok-Jin R, Yasuda Ryohei
机构信息
Department of Biochemistry, Duke University Medical Center, Durham, NC 27707, USA; Max Planck Florida Institute for Neuroscience, Jupiter, FL 33458, USA.
Max Planck Florida Institute for Neuroscience, Jupiter, FL 33458, USA.
出版信息
Neuron. 2017 May 17;94(4):800-808.e4. doi: 10.1016/j.neuron.2017.04.041.
CaMKII plays a critical role in decoding calcium (Ca) signals to initiate long-lasting synaptic plasticity. However, the properties of CaMKII that mediate Ca 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 Ca 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 CaMKII activity that is sufficient for inducing plasticity. Our findings demonstrate that Thr286 phosphorylation plays an important role in induction of LTP by integrating Ca signals, and it greatly promotes, but is dispensable for, the activation of CaMKII and LTP.
钙/钙调蛋白依赖性蛋白激酶II（CaMKII）在解码钙（Ca）信号以启动持久的突触可塑性方面起着关键作用。然而，介导棘突中Ca信号的CaMKII的特性仍然不清楚。在这里，我们使用快速成像双光子荧光寿命成像测量了棘突中的CaMKII活性。在重复性Ca升高期间的每个脉冲之后，CaMKII活性以逐步方式增加。苏氨酸286（Thr286）磷酸化减缓了CaMKII的衰减，从而将诱导棘突可塑性所需的频率降低了几倍。在没有Thr286磷酸化的情况下，增加刺激频率会导致高峰值突变型CaMKII活性，这足以诱导可塑性。我们的研究结果表明，Thr286磷酸化通过整合Ca信号在长时程增强（LTP）的诱导中起重要作用，并且它极大地促进了CaMKII的激活和LTP，但不是必需的。
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