Presynaptic calcium dynamics during short-term plasticity

神经元之间的信息传递是通过突触接触进行的，信息是由神经递质释放的时间特性和数量来编码的。神经递质的释放受到突触前钙离子浓度变化的严格调控。突触前活动导致各种类型的钙通道的激活，因此钙从细胞外来源进入末端，此外钙也可以以活动依赖性方式从细胞内池释放。 钙浓度的动态变化赋予终端以多种释放模式操作的能力。长期以来，人们一直认为突触前的这些不同的工作模式可以用钙离子浓度的变化来解释。相反，在本提案中，我们提议检验以下假设：

Communication between neurons occurs via synaptic contacts, information is coded by the temporal properties and the quantity of neurotransmitter release. Neurotramsitter release is tightly regulated and controlled by changes in presynaptic calcium concentration. Presynaptic activity leads to the activation of various types of calcium channels and hence calcium entry to the terminal from extracellular sources, in addition calcium can also be released from intracellular pools in an activity-dependent fashion. Dynamic changes in calcium concentration endow the terminal with the ability to operate at a wide variety of release modes. It has been long believed that that these various modes of presynaptic operation can be explained by changes in calcium concentration. In contrast, in the current proposal we propose to test the following hypothesis: