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首页> 外文期刊>Journal of Neurophysiology >Noise-induced hyperactivity in the inferior colliculus: Its relationship with hyperactivity in the dorsal cochlear nucleus
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Noise-induced hyperactivity in the inferior colliculus: Its relationship with hyperactivity in the dorsal cochlear nucleus

机译：噪声诱导的较差小学中的多动：其与背部耳蜗核的多动关系

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Intense noise exposure causes hyperactivity to develop in the mammalian dorsal cochlear nucleus (DCN) and inferior colliculus (IC). It has not yet been established whether the IC hyperactivity is driven by hyperactivity from extrinsic sources that include the DCN or instead is maintained independently of this input. We have investigated the extent to which IC hyperactivity is dependent on input from the contralateral DCN by comparing recordings of spontaneous activity in the IC of noise-exposed and control hamsters before and after ablation of the contralateral DCN. One group of animals was binaurally exposed to intense sound (10 kHz, 115 dB SPL, 4 h), whereas the control group was not. Both groups were studied electrophysiologically 2-3 wk later by first mapping spontaneous activity along the tonotopic axis of the IC to confirm induction of hyperactivity. Spontaneous activity was then recorded at a hyperactive IC locus over two 30-min periods, one with DCNs intact and the other after ablation of the contralateral DCN. In a subset of animals, activity was again mapped along the tonotopic axis after the time course of the activity was recorded before and after DCN ablation. Following recordings, the brains were fixed, and histological evaluations were performed to assess the extent of DCN ablation. Ablation of the DCN resulted in major reductions of IC hyperactivity. Levels of postablation activity in exposed animals were similar to the levels of activity in the IC of control animals, indicating an almost complete loss of hyperactivity in exposed animals. The results suggest that hyperactivity in the IC is dependent on support from extrinsic sources that include and may even begin with the DCN. This finding does not rule out longer term compensatory or homeostatic adjustments that might restore hyperactivity in the IC over time. ? 2012 the American Physiological Society.
机译：强烈的噪声暴露导致哺乳动物背耳核（DCN）和劣质胚轴（IC）中发育的多动。尚未确定IC多动症是否由来自包括DCN的外部源的多动因子驱动，或者是独立于此输入保持的。我们已经研究了IC多动取决于对侧DCN的输入，通过比较噪声暴露和控制仓鼠的IC中的自发活性记录，在对侧DCN之前和之后进行了比较。一组动物被分叉暴露于激烈的声音（10kHz，115 dB SPL，4小时），而对照组不是。通过沿IC的迂回轴线首先绘制自发性活性来研究两组两组，以确认诱导多动。然后在两个30分钟的时间内记录自发性活性，在两个30分钟的时间内，一个具有DCNS完好的一个，并且在混合后的DCN之后另一个。在动物的一部分中，在DCN消融之前和之后的活性的时间过程之后再次沿音调轴映射活性。在录制之后，脑子是固定的，进行组织学评价以评估DCN消融的程度。消融DCN导致IC多动的主要减少。暴露的动物的后水平活性水平类似于对照动物的IC中的活性水平，表明在暴露的动物中几乎完全丧失过度活动。结果表明，IC中的多动取决于内在源的支持，包括和甚至可以与DCN开始。这一发现并不能排除长期补偿或稳态调整，这些调整可能会随着时间的推移恢复IC中的多动。还是2012年美国生理社会。

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