Zeng Shangyou, Holmes William R
College of Electronic Engineering, Guangxi Normal University, Guangxi, China.
J Neurophysiol. 2010 Apr;103(4):1798-808. doi: 10.1152/jn.91235.2008. Epub 2010 Jan 27.
Activation of calcium-calmodulin dependent protein kinase II (CaMKII) during induction of long-term potentiation (LTP) is a series of complicated stochastic processes that are affected by noise. There are two main sources of noise affecting CaMKII activation within a dendritic spine. One is the noise associated with stochastic opening of N-methyl-d-aspartate (NMDA) receptor channels and the other is the noise associated with the stochastic reaction-diffusion kinetics leading to CaMKII activation. Many models have been developed to simulate CaMKII activation, but there is no fully stochastic model that studies the effect of noise on CaMKII activation. Here we construct a fully stochastic model to study these effects. Our results show that noise has important effects on CaMKII activation variability, with the effect from stochastic opening of NMDA receptor channels being 5-10 times more significant than that from stochastic reactions involving CaMKII. In addition, CaMKII activation levels and the variability of activation are greatly affected by small changes in NMDA receptor channel number at the synapse. One reason LTP induction protocols may require tetanic or repeated burst stimulation is that there is a need to overcome inherent variability to provide sufficiently large calcium signals through NMDA receptor channels; with meaningful physiological stimuli, noise may allow the calcium signal to exceed threshold for CaMKII activation when it might not do so otherwise.
在长时程增强(LTP)诱导过程中,钙调蛋白依赖性蛋白激酶II(CaMKII)的激活是一系列受噪声影响的复杂随机过程。在树突棘内影响CaMKII激活的噪声主要有两个来源。一个是与N-甲基-D-天冬氨酸(NMDA)受体通道随机开放相关的噪声,另一个是与导致CaMKII激活的随机反应扩散动力学相关的噪声。已经开发了许多模型来模拟CaMKII的激活,但尚无研究噪声对CaMKII激活影响的完全随机模型。在此,我们构建了一个完全随机模型来研究这些影响。我们的结果表明,噪声对CaMKII激活变异性有重要影响,NMDA受体通道随机开放产生的影响比涉及CaMKII的随机反应产生的影响大5至10倍。此外,突触处NMDA受体通道数量的微小变化会极大地影响CaMKII的激活水平和激活变异性。LTP诱导方案可能需要强直或重复爆发刺激的一个原因是,需要克服内在变异性,以通过NMDA受体通道提供足够大的钙信号;在有意义的生理刺激下,噪声可能使钙信号超过CaMKII激活阈值,否则可能无法达到该阈值。