Department of Physiology and Pharmacology, University of Calgary, Calgary, AB, Canada; Department of Psychology, University of Calgary, Calgary, AB, Canada.
Hear Res. 2013 Feb;296:121-30. doi: 10.1016/j.heares.2012.11.006. Epub 2012 Nov 12.
Persistent, passive exposure of adult cats to bandlimited tone pip ensembles or sharply-filtered white noise at moderate levels (∼70 dB SPL) leads to a long-term suppression of spontaneous and sound-evoked activity in the region(s) of primary auditory cortex (AI) normally tuned to the exposure spectrum, and to an enhancement of activity in one or more neighboring regions of AI, all in the apparent absence of hearing loss. Here, we first examined the effects of passive exposure to a more structured, real-world noise, consisting of a mix of power tool and construction sounds. This "factory noise" had less pronounced effects on adult cat AI than our previous random tone pip ensembles and white noise, and these effects appeared limited to the region of AI tuned to frequencies near the sharp factory noise cutoff at 16 kHz. To further investigate the role of sharp spectral edges in passive exposure-induced cortical plasticity, a second group of adult cats was exposed to a tone pip ensemble with a flat spectrum between 2 and 4 kHz and shallow cutoff slopes (12 dB/oct) on either side. Compared to our previous ensemble with the same power in the 2-4 kHz band but very steep slopes, exposure to the overall more intense, sloped stimulus had much weaker effects on AI. Finally, we explored the issue of exposure stimulus spectrotemporal density and found that low aggregate tone pip presentation rates of about one per second sufficed to induce changes in the adult AI similar to those characteristic of our previous, much denser exposures. These results are discussed in light of the putative mechanisms underlying exposure-induced auditory cortical plasticity, and the potential adverse consequences of working or living in moderately noisy environments.
成年猫持续被动暴露于限带音调pip 组合或适度水平的锐截止白噪声（约 70 dB SPL）会导致初级听觉皮层（AI）中正常调谐至暴露频谱的区域的自发和声音诱发活动长期抑制，并增强 AI 中一个或多个相邻区域的活动，而所有这些都明显没有听力损失。在这里，我们首先研究了被动暴露于更具结构性的实际噪声的影响，该噪声由电动工具和建筑声音的混合组成。与我们之前的随机音调 pip 组合和白噪声相比，这种“工厂噪声”对成年猫 AI 的影响较小，并且这些影响似乎仅限于调谐至 16 kHz 附近的尖锐工厂噪声截止频率的 AI 区域。为了进一步研究尖锐光谱边缘在被动暴露诱导皮质可塑性中的作用，第二组成年猫被暴露于具有 2 至 4 kHz 之间平坦频谱和浅截止斜率（12 dB/oct）的音调 pip 组合。与我们之前在 2-4 kHz 频带中具有相同功率但斜率非常陡峭的组合相比，暴露于整体强度更大、斜率较浅的刺激对 AI 的影响要小得多。最后，我们探讨了暴露刺激的光谱时间密度问题，发现每秒钟大约一个的低总音调 pip 呈现率足以引起与我们之前更密集暴露相似的成年 AI 变化。这些结果是根据潜在的暴露诱导听觉皮质可塑性的机制以及在适度嘈杂的环境中工作或生活的潜在不利后果进行讨论的。
