Institute for Auditory Neuroscience and InnerEarLab, University Medical Center Göttingen, Göttingen, Germany.
Collaborative Research Center, University of Göttingen, Göttingen, Germany.
Elife. 2018 Jan 12;7:e29275. doi: 10.7554/eLife.29275.
We studied the role of the synaptic ribbon for sound encoding at the synapses between inner hair cells (IHCs) and spiral ganglion neurons (SGNs) in mice lacking RIBEYE (RBE). Electron and immunofluorescence microscopy revealed a lack of synaptic ribbons and an assembly of several small active zones (AZs) at each synaptic contact. Spontaneous and sound-evoked firing rates of SGNs and their compound action potential were reduced, indicating impaired transmission at ribbonless IHC-SGN synapses. The temporal precision of sound encoding was impaired and the recovery of SGN-firing from adaptation indicated slowed synaptic vesicle (SV) replenishment. Activation of Ca-channels was shifted to more depolarized potentials and exocytosis was reduced for weak depolarizations. Presynaptic Ca-signals showed a broader spread, compatible with the altered Ca-channel clustering observed by super-resolution immunofluorescence microscopy. We postulate that RIBEYE disruption is partially compensated by multi-AZ organization. The remaining synaptic deficit indicates ribbon function in SV-replenishment and Ca-channel regulation.
我们研究了在缺乏 RIBEYE(RBE)的小鼠中,突触核糖体内耳毛细胞(IHC)和螺旋神经节神经元(SGN)之间突触的声音编码作用。电子和免疫荧光显微镜显示,每个突触接触处缺乏突触核糖和几个小活性区(AZ)的组装。SGN 的自发和声音诱发的放电率及其复合动作电位降低,表明无核糖的 IHC-SGN 突触的传递受损。声音编码的时间精度受损,从适应中恢复 SGN 放电表明 SV 补充速度较慢。Ca 通道的激活被转移到更去极化的电位,并且对于弱去极化,胞吐作用减少。 与超分辨率免疫荧光显微镜观察到的改变的 Ca 通道聚类一致, 前突触 Ca 信号显示出更广泛的扩散。我们推测 RIBEYE 破坏部分由多 AZ 组织补偿。 剩余的突触缺陷表明核糖在 SV 补充和 Ca 通道调节中的作用。