Foster Kelly A, Regehr Wade G
Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.
Neuron. 2004 Jul 8;43(1):119-31. doi: 10.1016/j.neuron.2004.06.022.
Many types of synapses throughout the nervous system are transiently depressed during high-frequency stimulation. Several mechanisms have been proposed to account for this depression, including depletion of release-ready vesicles. However, numerous studies have raised doubts about the importance of depletion in depression of central synapses and have implicated alternative mechanisms, such as decreased release probability. We use variance-mean analysis to determine the mechanism of depression at the climbing fiber to Purkinje cell synapse. We find that postsynaptic receptor saturation makes it difficult to distinguish between a decrease in available vesicles and a reduction in release probability. When AMPA receptor saturation is relieved with a low-affinity antagonist, variance-mean analysis reveals that depression arises from a decrease in the number of release-ready vesicles. Vesicle depletion is prominent, despite numerous docked vesicles at each release site, due to multivesicular release. We conclude that vesicle depletion can contribute significantly to depression of central synapses.
在整个神经系统中,许多类型的突触在高频刺激期间会短暂抑制。已经提出了几种机制来解释这种抑制,包括释放准备好的囊泡的耗尽。然而,大量研究对耗尽在中枢突触抑制中的重要性提出了质疑,并暗示了其他机制,如释放概率降低。我们使用方差均值分析来确定攀缘纤维与浦肯野细胞突触处抑制的机制。我们发现,突触后受体饱和使得区分可用囊泡数量的减少和释放概率的降低变得困难。当用低亲和力拮抗剂缓解AMPA受体饱和时,方差均值分析表明抑制源于释放准备好的囊泡数量的减少。尽管每个释放位点有大量停靠的囊泡,但由于多泡释放,囊泡耗尽很明显。我们得出结论,囊泡耗尽可对中枢突触的抑制有显著贡献。