Mulders W H A M, Spencer T C, Robertson D
The Auditory Laboratory, School of Anatomy, Physiology and Human Biology, The University of Western Australia, 35 Stirling Highway, Crawley WA 6009, Australia.
The Auditory Laboratory, School of Anatomy, Physiology and Human Biology, The University of Western Australia, 35 Stirling Highway, Crawley WA 6009, Australia.
Hear Res. 2016 May;335:128-137. doi: 10.1016/j.heares.2016.03.001. Epub 2016 Mar 10.
Partial hearing loss induced by acoustic trauma has been shown in animal models to result in an increased spontaneous firing rate in central auditory structures. This so-called hyperactivity has been suggested to be involved in the generation of tinnitus, a phantom auditory sensation. Although there is no universal cure for tinnitus, electrical stimulation of the cochlea, as achieved by a cochlear implant, can result in significant reduction of the tinnitus percept. However, the mechanism by which this tinnitus suppression occurs is as yet unknown and furthermore cochlear implantation may not be an optimal treatment option for tinnitus sufferers who are not profoundly deaf. A better understanding of the mechanism of tinnitus suppression by electrical stimulation of the cochlea, may lead to the development of more specialised devices for those for whom a cochlear implant is not appropriate. This study aimed to investigate the effects of electrical stimulation in the form of brief biphasic shocks delivered to the round window of the cochlea on the spontaneous firing rates of hyperactive inferior colliculus neurons following acoustic trauma in guinea pigs. Effects during the stimulation itself included both inhibition and excitation but spontaneous firing was suppressed for up to hundreds of ms after the cessation of the shock train in all sampled hyperactive neurons. Pharmacological block of olivocochlear efferent action on outer hair cells did not eliminate the prolonged suppression observed in inferior colliculus neurons, and it is therefore likely that activation of the afferent pathways is responsible for the central effects observed.
在动物模型中已表明，由声创伤引起的部分听力损失会导致中枢听觉结构的自发放电率增加。这种所谓的活动亢进被认为与耳鸣（一种幻听感觉）的产生有关。尽管耳鸣尚无通用的治愈方法，但通过人工耳蜗实现的耳蜗电刺激可显著减轻耳鸣感知。然而，这种耳鸣抑制发生的机制尚不清楚，此外，对于并非极重度耳聋的耳鸣患者，人工耳蜗植入可能不是最佳治疗选择。更好地理解耳蜗电刺激抑制耳鸣的机制，可能会为那些不适合人工耳蜗植入的患者开发出更专门的设备。本研究旨在探讨以短暂双相电刺激形式施加于豚鼠耳蜗圆窗对声创伤后下丘神经元自发放电率的影响。刺激过程中的影响包括抑制和兴奋，但在所有采样的活动亢进神经元中，在电刺激序列停止后，自发放电被抑制长达数百毫秒。对支配外毛细胞的橄榄耳蜗传出神经作用进行药理学阻断并不能消除在下丘神经元中观察到的长时间抑制，因此，传入通路的激活可能是观察到的中枢效应的原因。
