Schaette Roland, Kempter Richard
Institute for Theoretical Biology, Department of Biology, Humboldt-Universität zu Berlin, Invalidenstr. 43, 10115 Berlin, Germany.
Hear Res. 2008 Jun;240(1-2):57-72. doi: 10.1016/j.heares.2008.02.006. Epub 2008 Feb 26.
Cochlear damage can change the spontaneous firing rates of neurons in the dorsal cochlear nucleus (DCN). Increased spontaneous firing rates (hyperactivity) after acoustic trauma have been observed in the DCN of rodents such as hamsters, chinchillas and rats. This hyperactivity has been interpreted as a neural correlate of tinnitus. In cats, however, the spontaneous firing rates of DCN neurons were not significantly elevated after acoustic trauma. Species-specific spontaneous firing rates after cochlear damage might be attributable to differences in the response types of DCN neurons: In gerbils, type III response characteristics are predominant, whereas in cats type IV responses are more frequent. To address the question of how the development of hyperactivity after cochlear damage depends on the response type of DCN neurons, we use a computational model of the basic circuit of the DCN. By changing the strength of two types of inhibition, we can reproduce salient features of the responses of DCN neurons. Simulated cochlear damage, which decreases the activity of auditory nerve fibers, is assumed to activate homeostatic plasticity in projection neurons (PNs) of the DCN. We find that the resulting spontaneous firing rates depend on the response type of DCN PNs: PNs with type III and type IV-T response characteristics may become hyperactive, whereas type IV PNs do not develop increased spontaneous firing rates after acoustic trauma. This theoretical framework for the mechanisms and circumstances of the development of hyperactivity in central auditory neurons might also provide new insights into the development of tinnitus.
耳蜗损伤可改变耳蜗背核（DCN）中神经元的自发放电率。在仓鼠、毛丝鼠和大鼠等啮齿动物的DCN中，已观察到声学创伤后自发放电率增加（活动亢进）。这种活动亢进被解释为耳鸣的神经关联。然而，在猫中，声学创伤后DCN神经元的自发放电率并未显著升高。耳蜗损伤后物种特异性的自发放电率可能归因于DCN神经元反应类型的差异：在沙鼠中，III型反应特征占主导，而在猫中IV型反应更为常见。为了解决耳蜗损伤后活动亢进的发展如何依赖于DCN神经元反应类型这一问题，我们使用了DCN基本电路的计算模型。通过改变两种抑制类型的强度，我们可以重现DCN神经元反应的显著特征。模拟的耳蜗损伤会降低听神经纤维的活动，假定其会激活DCN投射神经元（PNs）中的稳态可塑性。我们发现，由此产生的自发放电率取决于DCN PNs的反应类型：具有III型和IV - T型反应特征的PNs可能会变得活动亢进，而IV型PNs在声学创伤后不会出现自发放电率增加的情况。这种关于中枢听觉神经元活动亢进发展机制和情况的理论框架也可能为耳鸣的发展提供新的见解。
