Salicylate-induced peripheral auditory changes and tonotopic reorganization of auditory cortex.

Salicylate-induced peripheral auditory changes and tonotopic reorganization of auditory cortex.
复制标题

水杨酸酯引起的外围听觉变化和听觉皮层的调整重组。

DOI:
10.1016/j.neuroscience.2011.02.005
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发表时间:
2011-04-28
期刊:
影响因子:
3.3
通讯作者:
Salvi, R. J.
Salvi, R. J.
中科院分区:
医学3区
文献类型:
--
作者:
Stolzberg, D.;Chen, G. -D.;Allman, B. L.;Salvi, R. J.

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耳鸣幻听的神经机制目前仍不清楚。超过25年来,大鼠急性水杨酸中毒后的暂时性耳鸣一直被用作了解幻音如何产生的模型。行为学研究表明,水杨酸诱导的大鼠耳鸣的音高约为16 kHz。为了更好地了解耳鸣音高的起源,在本研究中,在听觉输入和输出水平进行测量;在氯胺酮/甲苯噻嗪麻醉大鼠中进行耳蜗和皮层生理记录。复合动作电位和畸变产物耳声发射测量均显示水杨酸诱导的带通样耳蜗缺陷,其中耳蜗输入的减少在16 kHz时最少,在高频和低频时显著更大。在另一组大鼠中,使用多通道微电极跟踪初级听觉皮层神经元的频率感受野,在系统性水杨酸治疗前后。跟踪水杨酸盐后的频率感受野揭示了一群神经元,它们改变了它们的最大灵敏度频率(即,特征频率)朝向音调定位轴的耳鸣频率区域(~16 kHz)。本文所提供的数据支持这一假设,即水杨酸引起的耳鸣是由耳蜗输入的改变所决定的耳鸣音高的扩大的皮质表征引起的。此外,在水杨酸引起的耳鸣中,皮层频率感受野的柔韧性可能是由于水杨酸对皮层内抑制网络的直接作用。水杨酸盐后听觉皮层中中频的这种不成比例的表现可能导致该区域内信号的更精细分析,这可能在病理上增强集中在耳鸣频率处的假神经元活动的功能重要性。
The neuronal mechanism underlying the phantom auditory perception of tinnitus remains at present elusive. For over 25 years, temporary tinnitus following acute salicylate intoxication in rats has been used as a model to understand how a phantom sound can be generated. Behavioral studies have indicated the pitch of salicylate-induced tinnitus in the rat is approximately 16 kHz. In order to better understand the origin of the tinnitus pitch, in the present study, measurements were made at the levels of auditory input and output; both cochlear and cortical physiological recordings were performed in ketamine/xylazine anesthetized rats. Both compound action potentials and distortion product otoacoustic emission measurements revealed a salicylate-induced band-pass-like cochlear deficit in which the reduction of cochlear input was least at 16 kHz and significantly greater at high and low frequencies. In a separate group of rats, frequency receptive fields of primary auditory cortex neurons were tracked using multichannel microelectrodes before and after systemic salicylate treatment. Tracking frequency receptive fields following salicylate revealed a population of neurons that shifted their frequency of maximum sensitivity (i.e., characteristic frequency) towards the tinnitus frequency region of the tonotopic axis (~16 kHz). The data presented here supports the hypothesis that salicylateinduced tinnitus results from an expanded cortical representation of the tinnitus pitch determined by an altered profile of input from the cochlea. Moreover, the pliability of cortical frequency receptive fields during salicylate-induced tinnitus is likely due to salicylate’s direct action on intracortical inhibitory networks. Such a disproportionate representation of middle frequencies in the auditory cortex following salicylate may result in a finer analysis of signals within this region which may pathologically enhance the functional importance of spurious neuronal activity concentrated at tinnitus frequencies.
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发表时间: 2005-08-01
期刊: HEARING RESEARCH
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影响因子: --
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