Rosenmund Christian, Sigler Albrecht, Augustin Iris, Reim Kerstin, Brose Nils, Rhee Jeong Seop
Max-Planck-Institut für Biophysikalische Chemie, Abteilung Membranbiophysik, Am Fassberg 11, D-37077, Göttingen, Germany.
Neuron. 2002 Jan 31;33(3):411-24. doi: 10.1016/s0896-6273(02)00568-8.
Presynaptic short-term plasticity is an important adaptive mechanism regulating synaptic transmitter release at varying action potential frequencies. However, the underlying molecular mechanisms are unknown. We examined genetically defined and functionally unique axonal subpopulations of synapses in excitatory hippocampal neurons that utilize either Munc13-1 or Munc13-2 as synaptic vesicle priming factor. In contrast to Munc13-1-dependent synapses, Munc13-2-driven synapses show pronounced and transient augmentation of synaptic amplitudes following high-frequency stimulation. This augmentation is caused by a Ca(2+)-dependent increase in release probability and releasable vesicle pool size, and requires phospholipase C activity. Thus, differential expression of Munc13 isoforms at individual synapses represents a general mechanism that controls short-term plasticity and contributes to the heterogeneity of synaptic information coding.
突触前短期可塑性是一种重要的适应性机制，可在不同动作电位频率下调节突触递质释放。然而，其潜在的分子机制尚不清楚。我们研究了兴奋性海马神经元中利用Munc13-1或Munc13-2作为突触囊泡启动因子的、基因定义且功能独特的突触轴突亚群。与依赖Munc13-1的突触不同，由Munc13-2驱动的突触在高频刺激后显示出明显且短暂的突触幅度增强。这种增强是由释放概率和可释放囊泡池大小的钙依赖性增加引起的，并且需要磷脂酶C活性。因此，单个突触处Munc13亚型的差异表达代表了一种控制短期可塑性并有助于突触信息编码异质性的一般机制。
