The Auditory Laboratory, Discipline of Physiology, School of Biomedical, Biomolecular and Chemical Sciences, The University of Western Australia, 35 Stirling Highway, Crawley, Western Australia 6009, Australia.
Neuroscience. 2009 Dec 1;164(2):733-46. doi: 10.1016/j.neuroscience.2009.08.036. Epub 2009 Aug 20.
Plasticity in the adult mammalian brain can occur after damage to peripheral nerves and has also been described in the auditory system. Acoustic trauma, resulting in a loss of cochlear sensitivity, can lead to elevated levels of spontaneous activity, that is hyperactivity, in central nuclei such as the inferior colliculus. The current view is that this hyperactivity is centrally generated as a result of altered input. We investigated acute and chronic effects of acoustic trauma on cochlear sensitivity and development of hyperactivity in the inferior colliculus of guinea pigs. In addition, we investigated whether hyperactivity in the inferior colliculus, once established, is dependent on neural activity in the cochlea. Acoustic trauma (1 h continuous, 10 kHz tone at 124 dB SPL) resulted in a small but permanent, frequency restricted threshold loss in the cochlea up to 6 weeks post-exposure (maximum recovery time used). This was accompanied by hyperactivity in restricted frequency areas of the inferior colliculus, broadly corresponding to the cochlear threshold loss. We found that hyperactivity in the inferior colliculus depended on neural activity in the cochlea at all recovery times, since it disappeared after cochlear ablation and treatments blocking spontaneous firing of primary afferents. We suggest that the dependency of the central hyperactivity on the integrity of the peripheral receptor indicates hyperexcitability within the CNS resulting in greater neuronal firing in response to normal levels of peripheral spontaneous activity.
哺乳动物大脑在周围神经损伤后会发生可塑性，在听觉系统中也有描述。声创伤导致耳蜗敏感性丧失，可导致中枢核如下丘中的自发性活动水平升高，即过度活跃。目前的观点是，这种过度活跃是由于输入改变而在中枢产生的。我们研究了声创伤对豚鼠耳蜗敏感性和下丘过度活跃发展的急性和慢性影响。此外，我们还研究了一旦下丘过度活跃形成，是否依赖于耳蜗中的神经活动。声创伤（1 小时连续，10 kHz 频率，124 dB SPL）导致暴露后 6 周内耳蜗出现小但永久性、频率受限的阈值损失（使用最长恢复时间）。这伴随着下丘中受限频率区域的过度活跃，大致与耳蜗阈值损失相对应。我们发现，下丘中的过度活跃依赖于耳蜗中的神经活动，因为在耳蜗消融和阻断初级传入自发放电的治疗后，它消失了。我们认为，中枢过度活跃对周围受体完整性的依赖性表明中枢神经系统内的过度兴奋性导致神经元对正常水平的外周自发性活动产生更大的放电。
