Calmodulin as a major calcium buffer shaping vesicular release and short-term synaptic plasticity: facilitation through buffer dislocation.
Calmodulin as a major calcium buffer shaping vesicular release and short-term synaptic plasticity: facilitation through buffer dislocation.
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DOI：
10.3389/fncel.2015.00239
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发表时间：
2015
影响因子：
5.3
通讯作者：
Volynski KE
中科院分区：
文献类型：
--
作者：
Timofeeva Y;Volynski KE
突触小泡的动作电位依赖性释放和突触的短期可塑性受到内源性钙缓冲液的动态调节，内源性钙缓冲液塑造了突触前突触的[钙]谱。钙调蛋白是最丰富的突触前蛋白之一，它与钙离子的结合速度比其他任何特征的内源性神经元钙缓冲液都要快。然而，钙调蛋白对突触前快钙动力学和囊泡释放的直接影响还没有详细的研究。通过对小兴奋性突触钙离子进出耦合的实验约束三维扩散模拟，我们发现，在生理相关浓度下，钙调素缓冲钙离子在抑制囊泡释放和调节突触短时可塑性方面起主导作用。我们还提出了一种新的、潜在的强大的短期促进机制，该机制基于钙离子依赖的钙调蛋白分子在活动区内从质膜上的动态错位。
Action potential-dependent release of synaptic vesicles and short-term synaptic plasticity are dynamically regulated by the endogenous Ca2+ buffers that shape [Ca2+] profiles within a presynaptic bouton. Calmodulin is one of the most abundant presynaptic proteins and it binds Ca2+ faster than any other characterized endogenous neuronal Ca2+ buffer. Direct effects of calmodulin on fast presynaptic Ca2+ dynamics and vesicular release however have not been studied in detail. Using experimentally constrained three-dimensional diffusion modeling of Ca2+ influx–exocytosis coupling at small excitatory synapses we show that, at physiologically relevant concentrations, Ca2+ buffering by calmodulin plays a dominant role in inhibiting vesicular release and in modulating short-term synaptic plasticity. We also propose a novel and potentially powerful mechanism for short-term facilitation based on Ca2+-dependent dynamic dislocation of calmodulin molecules from the plasma membrane within the active zone.
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