The Auditory Laboratory, Discipline of Physiology, School of Biomedical, Biomolecular and Chemical Sciences, The University of Western Australia, 35 Stirling Highway, Crawley, WA 6009, Australia.
Neuroscience. 2011 Sep 29;192:753-60. doi: 10.1016/j.neuroscience.2011.06.046. Epub 2011 Jun 24.
Partial hearing loss is known to cause increased spontaneous activity at several stages of the central auditory pathways, and this phenomenon has been suggested as a possible neural substrate for tinnitus, a phantom hearing sensation. One recent study in guinea pig has suggested that approximately 6 weeks after acoustic trauma, the increased spontaneous activity in inferior colliculus is not intrinsically generated in the central nucleus but is dependent on afferent input from the cochlea. This was unexpected in view of the fact that tinnitus in human patients can persist after severing of the auditory nerve. In this study, we show that when recovery time after acoustic trauma is extended to 8 and 12 weeks, cochlear ablation does not significantly decrease the increased spontaneous activity measured in the inferior colliculus. This result demonstrates for the first time that central hyperactivity that develops after acoustic trauma transitions from an early stage when it is dependent on continued peripheral afferent input to a later stage in which the hyperactivity is intrinsically generated within the central nervous system.
部分听力损失已知会导致中枢听觉通路的几个阶段的自发性活动增加，这种现象被认为是耳鸣（一种幻听）的可能神经基础。最近在豚鼠身上的一项研究表明，在声创伤后大约 6 周，下丘脑中增加的自发性活动不是在中枢核内固有产生的，而是依赖于耳蜗的传入输入。鉴于人类患者的耳鸣在切断听神经后仍能持续存在，这一事实令人意外。在这项研究中，我们表明，当声创伤后的恢复时间延长至 8 周和 12 周时，耳蜗消融并不会显著降低在下丘脑中测量到的增加的自发性活动。这一结果首次表明，声创伤后发展起来的中枢过度活跃状态从依赖持续的外周传入输入的早期阶段过渡到后期阶段，在后期阶段，中枢神经系统内固有地产生了过度活跃状态。
