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首页> 外文期刊>Neuron >Ca2+ buffer saturation underlies paired pulse facilitation in calbindin-D28k-containing terminals.
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Ca2+ buffer saturation underlies paired pulse facilitation in calbindin-D28k-containing terminals.

机译:Ca2 +缓冲液饱和是含calbindin-D28k末端中配对脉冲促进的基础。

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摘要

Ca2+ buffer saturation was proposed as a mechanism of paired pulse facilitation (PPF). However, whether it operates under native conditions remained unclear. Here we show that saturation of the endogenous fast Ca2+ buffer calbindin-D28k (CB) plays a major role in PPF at CB-containing synapses. Paired recordings from synaptically connected interneurons and pyramidal neurons in the mouse neocortex revealed that dialysis increased the amplitude of the first response and decreased PPF. Loading the presynaptic terminals with BAPTA or CB rescued the effect of the CB washout. We extended the study to the CB-positive facilitating excitatory mossy fiber-CA3 pyramidal cell synapse. The effects of different extracellular Ca2+ concentrations and of EGTA indicated that PPF in CB-containing terminals depended on Ca2+ influx rather than on the initial release probability. Experiments in CB knockout mice confirmed that buffer saturation is a novel basic presynaptic mechanism for activity-dependent control of synaptic gain.
机译:提出了Ca2 +缓冲液饱和作为配对脉冲促进(PPF)的机制。但是,是否在自然条件下运行尚不清楚。在这里,我们显示内源性快速Ca2 +缓冲液calbindin-D28k(CB)的饱和在含CB突触的PPF中起主要作用。小鼠新皮层中突触连接的神经元和锥体神经元的配对记录显示,透析增加了首次反应的幅度,降低了PPF。用BAPTA或CB装载突触前末端可拯救CB冲洗的效果。我们将研究扩展到CB阳性,促进兴奋性苔藓纤维-CA3锥体细胞突触。不同细胞外Ca2 +浓度和EGTA的影响表明,含CB的末端中的PPF取决于Ca2 +的流入量,而不是初始释放的可能性。在CB基因敲除小鼠中进行的实验证实,缓冲液饱和是一种新型的基本突触前机制,可用于活动依赖的突触增益控制。

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