阿米卡辛致耳蜗损伤的成年栗鼠听觉皮层的同种位定位。

A Kakigi, H Hirakawa, N Harel, R J Mount, R V Harrison
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引用次数: 27

摘要

我们发现,在阿米卡辛诱导的基底耳蜗损伤后,成年龙猫初级听觉皮层的tonotopic图(基于神经元反应阈值)发生了重组。我们发现一个频率的过度代表,对应于耳蜗病变的边界区域。观察到的重组在程度上与之前在发育模型中看到的相似。研究了过度表征区域内神经元的特性,以确定它们的反应是源于共同输入(真正可塑性的指示)还是仅仅代表了截断感觉上皮活动的结果(“伪可塑性”)。我们的数据的某些方面符合真正的可塑性模型,并表明成熟皮层的失传入皮层有可能重新获得与存活的感觉上皮的连接。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Tonotopic mapping in auditory cortex of the adult chinchilla with amikacin-induced cochlear lesions.

We have found a reorganization of tonotopic maps (based on neuron response thresholds) in primary auditory cortex of the adult chinchilla after amikacin-induced basal cochlear lesions. We find an over-representation of a frequency that corresponds to the border area of the cochlear lesion. The reorganization observed is similar in extent to that previously seen in a developmental model. The properties of neurons within the over-represented area were investigated in order to determine whether their responses originated from a common input (an indication of true plasticity) or represented only the result of truncating the activity of the sensory epithelium ("pseudo-plasticity"). Some aspects of our data fit with a true plasticity model and indicate the potential for the deafferented cortex of the mature cortex to regain connections with the surviving sensory epithelium.

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