Rybalko Natalia, Chumak Tetyana, Bureš Zbyněk, Popelář Jiří, Šuta Daniel, Syka Josef
Department of Auditory Neuroscience, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Vídeňská 1083, 142 20 Prague, Czech Republic.
Department of Auditory Neuroscience, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Vídeňská 1083, 142 20 Prague, Czech Republic.
Behav Brain Res. 2015 Jun 1;286:212-21. doi: 10.1016/j.bbr.2015.02.046. Epub 2015 Mar 5.
Even brief acoustic trauma during the critical period of development that results in no permanent hearing threshold shift may lead to altered auditory processing in adulthood. By monitoring the acoustic startle response (ASR), we examined the development of auditory function in control rats and in rats exposed to intense noise at the 14th postnatal day (P14). First ASRs appeared on P10-P11 to intense low-frequency tones. By P14, the range of sound intensities and frequencies eliciting ASRs extended considerably, the ASR reactivity being similar at all frequencies (4-32 kHz). During the subsequent two weeks, ASR amplitudes to low-frequency stimuli (4-8 kHz) increased, whereas the ASRs to high-frequency tones were maintained (16 kHz) or even decreased (32 kHz). Compared to controls, noise exposure on P14 (125 dB SPL for 8, 12, or 25 min) produced transient hyper-reactivity to startle stimuli, manifested by a decrease of ASR thresholds and an increase of ASR amplitudes. ASR enhancement occurred regardless of permanent hearing loss and was more pronounced at high frequencies. The hyper-reactivity of ASRs declined by P30; the ASR amplitudes in adult exposed rats were lower than in controls. The histological control did not reveal loss of hair cells in adult exposed rats, however, the number of inner hair cell ribbon synapses was significantly decreased, especially in the high-frequency part of the cochlea. The results indicate that early acoustic trauma may result in complex changes of ASRs during development.
即使在发育关键期发生的短暂性听觉创伤未导致永久性听力阈值改变，也可能在成年期导致听觉处理功能改变。通过监测听觉惊吓反应（ASR），我们研究了对照组大鼠以及在出生后第14天（P14）暴露于高强度噪声的大鼠的听觉功能发育情况。最初的ASR在P10 - P11时出现于高强度低频音调刺激下。到P14时，引发ASR的声音强度和频率范围显著扩大，所有频率（4 - 32 kHz）下的ASR反应性相似。在随后的两周内，低频刺激（4 - 8 kHz）引发的ASR幅度增加，而高频音调（16 kHz）引发的ASR保持不变甚至下降（32 kHz）。与对照组相比，P14时的噪声暴露（125 dB SPL，持续8、12或25分钟）使大鼠对惊吓刺激产生短暂的过度反应，表现为ASR阈值降低和ASR幅度增加。无论是否存在永久性听力损失，ASR增强均会出现，且在高频时更为明显。ASR的过度反应在P30时下降；成年期暴露大鼠的ASR幅度低于对照组。组织学检查未发现成年期暴露大鼠的毛细胞丢失，然而，内毛细胞带状突触的数量显著减少，尤其是在耳蜗的高频部分。结果表明，早期听觉创伤可能导致发育过程中ASR的复杂变化。
