Center for Hearing & Deafness, The State University of New York at Buffalo, NY 14214, USA.
Brain Res. 2012 Nov 16;1485:108-16. doi: 10.1016/j.brainres.2012.02.008. Epub 2012 Feb 9.
Hyperacusis, a marked intolerance to normal environmental sound, is a common symptom in patients with tinnitus, Williams syndrome, autism, and other neurologic diseases. It has been suggested that an imbalance of excitation and inhibition in the central auditory system (CAS) may play an important role in hyperacusis. Recent studies found that noise exposure, one of the most common causes of hearing loss and tinnitus, can increase the auditory cortex (AC) response, presumably by increasing the gain of the AC. However, it is not clear whether the increased cortical response will affect sound sensitivity and induce hyperacusis. In this experiment, we studied the effects of noise exposure (narrow band noise, 12 kHz, 120 dB SPL, 1 hour) on the physiological response of the inferior colliculus (IC) and the AC, and the behavioral sound reaction in conscious Sprague Dawley rats. Noise exposure induced a decrease of sound evoked potential in the IC. However, significant increases of AC response including sound evoked potentials and the spike firing rates of AC neurons were recorded right after the noise exposure. These results suggest that noise exposure induces hyperexcitability of AC presumably by increasing the post-synaptic response of AC neurons. The behavioral consequence of the noise exposure on sound perception was measured by the amplitude of the acoustic startle response before and after noise exposure in a separate group of rats. Although noise exposure caused a moderate hearing loss, the acoustic startle amplitude at the super-threshold level was significantly increased. These results suggest that noise exposure can cause exaggerated the sound reaction which may be related with the enhanced responsiveness of the AC neurons. This phenomenon may be related with noise induced hyperacusis.This article is part of a Special Issue entitled: Tinnitus Neuroscience.
听觉过敏，即对正常环境声音的显著不耐受，是耳鸣、威廉姆斯综合征、自闭症和其他神经疾病患者的常见症状。有研究表明，中枢听觉系统（central auditory system，CAS）中兴奋和抑制的失衡可能在听觉过敏中发挥重要作用。最近的研究发现，噪声暴露是听力损失和耳鸣的最常见原因之一，它可以增加听觉皮层（auditory cortex，AC）的反应，可能是通过增加 AC 的增益来实现的。然而，目前尚不清楚增加的皮质反应是否会影响声音敏感度并导致听觉过敏。在本实验中，我们研究了噪声暴露（窄带噪声，12 kHz，120 dB SPL，1 小时）对意识状态下 Sprague Dawley 大鼠下丘（inferior colliculus，IC）和 AC 的生理反应以及对声音反应行为的影响。噪声暴露导致 IC 中声音诱发电位减小。然而，在噪声暴露后，AC 的反应包括声音诱发电位和 AC 神经元的尖峰放电率都显著增加。这些结果表明，噪声暴露通过增加 AC 神经元的突触后反应，导致 AC 的兴奋性增加。在另一组大鼠中，通过测量噪声暴露前后声惊反射的幅度来测量噪声暴露对声音感知的行为后果。尽管噪声暴露导致中度听力损失，但超阈值水平的声惊反射幅度显著增加。这些结果表明，噪声暴露会导致声音反应过度，这可能与 AC 神经元的反应增强有关。这种现象可能与噪声诱导的听觉过敏有关。本文是一个特刊的一部分，特刊主题为：耳鸣神经科学。
