Habets Ron L P, Borst J Gerard G
Erasmus MC, University Medical Center Rotterdam, Dr. Molewaterplein 50, 3015 GE Rotterdam, The Netherlands.
J Neurophysiol. 2006 Dec;96(6):2868-76. doi: 10.1152/jn.00427.2006. Epub 2006 Aug 9.
We studied the contribution of a change in presynaptic calcium influx to posttetanic potentiation (PTP) in the calyx of Held synapse, an axosomatic synapse in the auditory brain stem. We made whole cell patch-clamp recordings of a principal cell after loading of the presynaptic terminal with a calcium dye. After induction of PTP by a high-frequency train of afferent stimuli, the Fluo-4 fluorescence transients evoked by an action potential became on average 15 +/- 4% larger (n = 7). Model predictions did not match the fluorescence transients evoked by trains of brief calcium currents unless the endogenous calcium buffer had low affinity for calcium, making a contribution of saturation of the endogenous buffer to the synaptic potentiation we observed in the present experiments less likely. Our data therefore suggest that the increase of release probability during PTP at the calyx of Held synapse is largely explained by an increase in the calcium influx per action potential.
我们研究了突触前钙内流变化对听神经脑干轴体突触——Held壶腹突触强直后增强(PTP)的作用。在用钙染料加载突触前终末后,我们对主细胞进行了全细胞膜片钳记录。在通过高频传入刺激诱导PTP后,动作电位诱发的Fluo-4荧光瞬变平均增大了15±4%(n = 7)。除非内源性钙缓冲剂对钙的亲和力较低,否则模型预测与短暂钙电流序列诱发的荧光瞬变不匹配,这使得内源性缓冲剂饱和对我们在本实验中观察到的突触增强作用的贡献不太可能。因此,我们的数据表明,Held壶腹突触PTP期间释放概率的增加很大程度上是由每个动作电位钙内流的增加所解释的。