Short-term plasticity preserves a brief history of synaptic activity that is communicated to the postsynaptic neuron. This is primarily regulated by a calcium signal initiated by voltage dependent calcium channels in the presynaptic terminal. Imaging studies of CA3-CA1 synapses reveal the presence of another source of calcium, the endoplasmic reticulum (ER) in all presynaptic terminals. However, the precise role of the ER in modifying STP remains unexplored. We performed in-silico experiments in synaptic geometries based on reconstructions of the rat CA3-CA1 synapses to investigate the contribution of ER. Our model predicts that presynaptic ER is critical in generating the observed short-term plasticity profile of CA3-CA1 synapses and allows synapses with low release probability to operate more reliably. Blocking the ER lowers facilitation in a manner similar to what has been previously characterized in animal models of Alzheimer’s disease and underscores the important role played by presynaptic stores in normal function.

短期可塑性保留了与突触后神经元通信的突触活动的简短历史。这主要由突触前末梢电压依赖性钙通道发起的钙信号调节。CA3-CA1 突触的成像研究揭示了另一种钙源的存在，即所有突触前末梢的内质网 (ER)。然而，ER 在修改 STP 中的确切作用仍未得到探索。我们基于大鼠 CA3-CA1 突触的重建在突触几何结构中进行了电子计算机实验，以研究 ER 的贡献。我们的模型预测，突触前 ER 对于生成观察到的 CA3-CA1 突触短期可塑性特征至关重要，并允许具有低释放概率的突触更可靠地运行。