Contribution of auditory nerve fibers to compound action potential of the auditory nerve
Contribution of auditory nerve fibers to compound action potential of the auditory nerve
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DOI：
10.1152/jn.00738.2013
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发表时间：
2014-09-01
影响因子：
2.5
通讯作者：
Wang, Jing
中科院分区：
文献类型：
--
作者：
Bourien, Jerome;Tang, Yong;Wang, Jing
声诱发复合动作电位（CAP）是听觉神经纤维（ANF）的同步激活，常用于实验和临床环境中探测耳聋。所有ANF都被认为有助于CAP阈值和振幅：低声压水平激活高自发频率（SR）纤维，并逐渐增加水平招募中等和低SR纤维。在这项研究中，我们定量分析的贡献，心钠素CAP 6天后，30分钟的哇巴因注入圆窗龛。解剖学检查显示，随着哇巴因浓度的增加，ANF逐渐消融。CAP振幅和阈值与ANF损失的关系显示了三个ANF库：1）高度哇巴因敏感的库，其不参与CAP阈值或振幅，2）不太敏感的库，其仅编码CAP振幅，和3）哇巴因抗性库，其为CAP阈值和振幅所需。值得注意的是，这三个池的分布类似于基于SR的ANF分布（低、中和高SR纤维），表明低SR纤维损失使CAP不受影响。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纤维的延迟和广泛的第一个尖峰潜伏期分布。除了解开编码CAP的神经机制外，我们对豚鼠ANF组装的计算模拟将我们的实验结果推广并扩展到不同物种的哺乳动物。总之，我们的数据表明，大量的ANF损失可以与正常的听阈共存，甚至不变的CAP振幅。
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.