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首页> 外文期刊>The European Journal of Neuroscience >Semaphorin 3A induces acute changes in membrane excitability in spiral ganglion neurons in vitro
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Semaphorin 3A induces acute changes in membrane excitability in spiral ganglion neurons in vitro

机译：Semaphorin 3a在体外螺旋神经节神经元中的膜兴奋性急性变化

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The development and survival of spiral ganglion neurons (SGNs) are dependent on multiple trophic factors as well as membrane electrical activity. Semaphorins (Sema) constitute a family of membrane-associated and secreted proteins that have garnered significant attention as a potential SGN "navigator" during cochlea development. Previous studies using mutant mice demonstrated that Sema3A plays a role in the SGN pathfinding. The mechanisms, however, by which Sema3A shapes SGNs firing behavior are not known. In these studies, we found that Sema3A plays a novel role in regulating SGN resting membrane potential and excitability. Using dissociated SGN from pre-hearing (P3-P5) and post-hearing mice (P12-P15), we recorded membrane potentials using whole-cell patch clamp recording techniques in apical and basal SGN populations. Recombinant Sema3A was applied to examine the effects on intrinsic membrane properties and action potentials evoked by current injections. Apical and basal SGNs from newborn mice treated with recombinant Sema3A (100 ng/ml) displayed a higher resting membrane potential, higher threshold, decreased amplitude, and prolonged latency and duration of spikes. Although a similar phenomenon was observed in SGNs from post-hearing mice, the resting membrane potential was essentially indistinguishable before and after Sema3A exposure. Sema3A-mediated changes in membrane excitability were associated with a significant decrease in K+ and Ca2+ currents. Sema3A acts through linopirdine-sensitive K+ channels in apical, but not in the basal SGNs. Therefore, Sema3A induces differential effects in SGN membrane excitability that are dependent on age and location, and constitutes an additional early and novel effect of Sema3A SGNs in vitro.
机译：螺旋神经节神经元（SGNS）的开发和存活取决于多种营养因素以及膜电活动。 Semaphorins（Sema）构成膜相关和分泌蛋白质的家族，在耳蜗发育过程中占据了潜在的SGN“导航仪”。以前使用突变小鼠的研究表明Sema3a在SGN Pathfinding中发挥作用。然而，该机制通过该机制，SEMA3A形状SGNS射击行为不知道。在这些研究中，我们发现Sema3a在调节SGN休息膜电位和兴奋方面发挥了新颖作用。使用解离的SGN从预听力（P3-P5）和听力后小鼠（P12-P15）中，我们在顶端和基础SGN群中使用全细胞膜片钳钳记录技术记录膜电位。施用重组SEMA3A以检测通过电流注射引起的内在膜性能和作用电位的影响。用重组Sema3a（100ng / ml）处理的新生小鼠的顶端和基础SgNs显示出较高的静止膜电位，更高的阈值，降低幅度和延长潜伏期和尖峰持续时间。尽管在听力后小鼠中观察到类似的现象，但在Sema3a暴露之前和之后，静止膜电位基本上是难以区分的。 Sema3a介导的膜兴奋性的变化与K +和Ca2 +电流的显着降低有关。 Sema3a通过顶端的LinoPirdine敏感K +通道作用，但不在基础SGNS中。因此，Sema3a在SGN膜兴奋性中诱导差异效应，其依赖于年龄和地点，并且在体外构成SEMA3A SGN的额外早期和新效果。

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