Bourien Jérôme, Tang Yong, Batrel Charlène, Huet Antoine, Lenoir Marc, Ladrech Sabine, Desmadryl Gilles, Nouvian Régis, Puel Jean-Luc, Wang Jing
Institut National de la Santé et de la Recherche Médicale UMR 1051, Institute for Neurosciences of Montpellier, Montpellier, France; University of Montpellier 1 and 2, Montpellier, France; and.
Institut National de la Santé et de la Recherche Médicale UMR 1051, Institute for Neurosciences of Montpellier, Montpellier, France; University of Montpellier 1 and 2, Montpellier, France; and Department of Otolaryngology, First Affiliated Hospital of Kunming Medical University, Kunming, China.
J Neurophysiol. 2014 Sep 1;112(5):1025-39. doi: 10.1152/jn.00738.2013. Epub 2014 May 21.
Sound-evoked compound action potential (CAP), which captures the synchronous activation of the auditory nerve fibers (ANFs), is commonly used to probe deafness in experimental and clinical settings. All ANFs are believed to contribute to CAP threshold and amplitude: low sound pressure levels activate the high-spontaneous rate (SR) fibers, and increasing levels gradually recruit medium- and then low-SR fibers. In this study, we quantitatively analyze the contribution of the ANFs to CAP 6 days after 30-min infusion of ouabain into the round window niche. Anatomic examination showed a progressive ablation of ANFs following increasing concentration of ouabain. CAP amplitude and threshold plotted against loss of ANFs revealed three ANF pools: 1) a highly ouabain-sensitive pool, which does not participate in either CAP threshold or amplitude, 2) a less sensitive pool, which only encoded CAP amplitude, and 3) a ouabain-resistant pool, required for CAP threshold and amplitude. Remarkably, distribution of the three pools was similar to the SR-based ANF distribution (low-, medium-, and high-SR fibers), suggesting that the low-SR fiber loss leaves the CAP unaffected. Single-unit recordings from the auditory nerve confirmed this hypothesis and further showed that it is due to the delayed and broad first spike latency distribution of low-SR fibers. In addition to unraveling the neural mechanisms that encode CAP, our computational simulation of an assembly of guinea pig ANFs generalizes and extends our experimental findings to different species of mammals. Altogether, our data demonstrate that substantial ANF loss can coexist with normal hearing threshold and even unchanged CAP amplitude.
声诱发复合动作电位（CAP）可捕捉听神经纤维（ANF）的同步激活，常用于实验和临床环境中探测耳聋情况。所有ANF都被认为对CAP阈值和幅度有贡献：低声压水平激活高自发放电率（SR）纤维，随着声压水平增加，逐渐募集中等SR纤维，然后是低SR纤维。在本研究中，我们定量分析了在圆窗龛内注入哇巴因30分钟后6天，ANF对CAP的贡献。解剖学检查显示，随着哇巴因浓度增加，ANF逐渐被消融。将CAP幅度和阈值与ANF损失情况作图，揭示了三个ANF池：1）一个对哇巴因高度敏感的池，它不参与CAP阈值或幅度的形成；2）一个较不敏感的池，它仅编码CAP幅度；3）一个对哇巴因有抗性的池，是CAP阈值和幅度所必需的。值得注意的是，这三个池的分布与基于SR的ANF分布（低、中、高SR纤维）相似；这表明低SR纤维的损失不会影响CAP。听神经的单单位记录证实了这一假设，并进一步表明这是由于低SR纤维的第一个峰潜伏期分布延迟且宽泛所致。除了解开编码CAP的神经机制外，我们对豚鼠ANF集合的计算模拟将我们的实验结果推广并扩展到了不同种类的哺乳动物。总之，我们的数据表明，大量的ANF损失可以与正常听力阈值甚至不变的CAP幅度同时存在。
