Biomedical Applications Group, Pittsburgh Supercomputing Center, Carnegie Mellon University, Pittsburgh, Pennsylvania; Joint Carnegie Mellon-University of Pittsburgh PhD Program in Computational Biology, School of Computer Science, Carnegie Mellon University, Pittsburgh, Pennsylvania;
Department of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania; and.
J Neurophysiol. 2015 Jan 1;113(1):71-87. doi: 10.1152/jn.00198.2014. Epub 2014 Sep 10.
Short-term synaptic facilitation occurs during high-frequency stimulation, is known to be dependent on presynaptic calcium ions, and persists for tens of milliseconds after a presynaptic action potential. We have used the frog neuromuscular junction as a model synapse for both experimental and computer simulation studies aimed at testing various mechanistic hypotheses proposed to underlie short-term synaptic facilitation. Building off our recently reported excess-calcium-binding-site model of synaptic vesicle release at the frog neuromuscular junction (Dittrich M, Pattillo JM, King JD, Cho S, Stiles JR, Meriney SD. Biophys J 104: 2751-2763, 2013), we have investigated several mechanisms of short-term facilitation at the frog neuromuscular junction. Our studies place constraints on previously proposed facilitation mechanisms and conclude that the presence of a second class of calcium sensor proteins distinct from synaptotagmin can explain known properties of facilitation observed at the frog neuromuscular junction. We were further able to identify a novel facilitation mechanism, which relied on the persistent binding of calcium-bound synaptotagmin molecules to lipids of the presynaptic membrane. In a real physiological context, both mechanisms identified in our study (and perhaps others) may act simultaneously to cause the experimentally observed facilitation. In summary, using a combination of computer simulations and physiological recordings, we have developed a stochastic computer model of synaptic transmission at the frog neuromuscular junction, which sheds light on the facilitation mechanisms in this model synapse.
短期突触易化发生在高频刺激期间,已知依赖于突触前钙离子,并在前动作电位后持续数十毫秒。我们使用蛙神经肌肉接头作为实验和计算机模拟研究的模型突触,旨在测试各种机械假说,这些假说被认为是短期突触易化的基础。在我们最近报道的关于蛙神经肌肉接头突触小泡释放的多余钙结合位点模型(Dittrich M、Pattillo JM、King JD、Cho S、Stiles JR、Meriney SD。Biophys J 104:2751-2763,2013)的基础上,我们研究了蛙神经肌肉接头的几种短期易化机制。我们的研究限制了以前提出的易化机制,并得出结论,存在第二种不同于突触结合蛋白的钙传感器蛋白可以解释在蛙神经肌肉接头观察到的已知易化特性。我们进一步能够确定一种新的易化机制,该机制依赖于与突触结合蛋白结合的钙离子分子与突触前膜脂质的持续结合。在真实的生理环境中,我们在研究中确定的两种机制(也许还有其他机制)可能同时作用导致实验观察到的易化。总之,我们使用计算机模拟和生理记录的组合,开发了一种蛙神经肌肉接头的突触传递随机计算机模型,该模型揭示了该模型突触中的易化机制。