Li Yang, Ropp Tessa-Jonne F, May Bradford J, Young Eric D
Department of Biomedical Engineering, Center for Hearing and Balance, Johns Hopkins University, 505 Traylor Bldg., 720 Rutland Ave., Baltimore, MD, 21205, USA,
J Assoc Res Otolaryngol. 2015 Aug;16(4):487-505. doi: 10.1007/s10162-015-0522-z. Epub 2015 May 13.
Acoustic trauma damages the cochlea but secondarily modifies circuits of the central auditory system. Changes include decreases in inhibitory neurotransmitter systems, degeneration and rewiring of synaptic circuits, and changes in neural activity. Little is known about the consequences of these changes for the representation of complex sounds. Here, we show data from the dorsal cochlear nucleus (DCN) of rats with a moderate high-frequency hearing loss following acoustic trauma. Single-neuron recording was used to estimate the organization of neurons' receptive fields, the balance of inhibition and excitation, and the representation of the spectra of complex broadband stimuli. The complex stimuli had random spectral shapes (RSSs), and the responses were fit with a model that allows the quality of the representation and its degree of linearity to be estimated. Tone response maps of DCN neurons in rat are like those in other species investigated previously, suggesting the same general organization of this nucleus. Following acoustic trauma, abnormal response types appeared. These can be interpreted as reflecting degraded tuning in auditory nerve fibers plus loss of inhibitory inputs in DCN. Abnormal types are somewhat more prevalent at later times (103-376 days) following the exposure, but not significantly so. Inhibition became weaker in post-trauma neurons that retained inhibitory responses but also disappeared in many neurons. The quality of the representation of spectral shape, measured by sensitivity to the spectral shapes of RSS stimuli, was decreased following trauma; in fact, neurons with abnormal response types responded mainly to overall stimulus level, and not spectral shape.
声创伤会损害耳蜗,但继而会改变中枢听觉系统的回路。这些变化包括抑制性神经递质系统的减少、突触回路的退化和重新布线,以及神经活动的改变。对于这些变化对复杂声音表征的影响知之甚少。在此,我们展示了声创伤后中度高频听力损失大鼠的背侧耳蜗核(DCN)的数据。使用单神经元记录来估计神经元感受野的组织、抑制和兴奋的平衡,以及复杂宽带刺激频谱的表征。复杂刺激具有随机频谱形状(RSS),并且用一个模型拟合反应,该模型可以估计表征的质量及其线性程度。大鼠DCN神经元的音调反应图谱与之前研究的其他物种相似,表明该核的一般组织相同。声创伤后出现了异常反应类型。这些可以解释为反映了听神经纤维调谐的退化以及DCN中抑制性输入的丧失。异常类型在暴露后的后期(103 - 376天)更为普遍,但差异不显著。创伤后保留抑制性反应的神经元中抑制作用变弱,但在许多神经元中抑制作用也消失了。创伤后,通过对RSS刺激频谱形状的敏感性来衡量的频谱形状表征质量下降;实际上,具有异常反应类型的神经元主要对整体刺激水平做出反应,而不是对频谱形状做出反应。