Laboratory of Molecular Synaptic Function, Graduate School of Brain Science, Doshisha University, Kyoto 610-0394, Japan; Department of Physiology, Faculty of Medicine, Osaka Medical College, Osaka 569-8686, Japan.
Society-Academia Collaboration for Innovation, Kyoto University, Kyoto 606-8501, Japan.
Cell Rep. 2018 Mar 20;22(12):3134-3141. doi: 10.1016/j.celrep.2018.02.080.
Synaptic efficacy plays crucial roles in neuronal circuit operation and synaptic plasticity. Presynaptic determinants of synaptic efficacy are neurotransmitter content in synaptic vesicles and the number of vesicles undergoing exocytosis at a time. Bursts of presynaptic firings depress synaptic efficacy, mainly due to depletion of releasable vesicles, whereas recovery from strong depression is initiated by endocytic vesicle retrieval followed by refilling of vesicles with neurotransmitter. We washed out presynaptic cytosolic GABA to induce a rundown of IPSCs at cerebellar inhibitory cell pairs in slices from rats and then allowed fast recovery by elevating GABA concentration using photo-uncaging. The time course of this recovery coincided with that of IPSCs from activity-dependent depression induced by a train of high-frequency stimulation. We conclude that vesicular GABA uptake can be a limiting step for the recovery of inhibitory neurotransmission from synaptic depression.
突触效能在神经元回路运作和突触可塑性中起着至关重要的作用。突触效能的突触前决定因素是突触小泡中的神经递质含量和一次发生胞吐作用的小泡数量。突触前的一连串放电会抑制突触效能，主要是由于可释放的小泡耗竭，而从强抑制中恢复则是由内吞小泡回收引发的，随后小泡用神经递质填充。我们冲洗掉小脑抑制性细胞对突触前胞质 GABA，以在大鼠脑片上诱导 IPSC 的衰减，然后通过光解笼控提高 GABA 浓度来快速恢复。这种恢复的时程与由高频刺激引发的依赖于活动的 IPSC 抑制性神经传递抑制的恢复时程相吻合。我们得出结论，囊泡 GABA 摄取可能是恢复抑制性神经传递从突触抑制中恢复的限制步骤。
