Pienkowski Martin, Eggermont Jos J
Department of Physiology and Pharmacology, University of Calgary, Calgary, Alta., Canada T2N 1N4.
Hear Res. 2009 Nov;257(1-2):24-40. doi: 10.1016/j.heares.2009.07.011. Epub 2009 Aug 6.
We recently reported that passive exposure for at least 4 months of adult cats to a two-octave-wide tone pip ensemble at 80 dB SPL, decreased the responsiveness of primary auditory cortex (AI) to sound frequencies in the exposure band, and increased the responsiveness to frequencies at the outer edges of the band. Here we expand on this by demonstrating qualitatively similar plasticity for a 6-week exposure level of 68 dB SPL. Though no peripheral hearing loss is induced by the exposure, the resulting reorganization of the AI tonotopic map resembles that following a restricted lesion of the sensory epithelium. Most exposure-induced effects were likely present in the thalamus, as deduced from changes in local field potentials, but were further modified in AI. We then examined the potential for the reversal of these changes, given recovery in a quiet laboratory environment for up to 12 weeks after the cessation of exposure. While frequency tuning returned to near-normal, other neuronal response properties, as well as tonotopic map organization, remained abnormal at the end of our 12-week window. This could have implications for persistently noisy work/recreation/living environments, even at levels considerably below those presently considered unacceptable.
我们最近报告称,成年猫在80分贝声压级下被动暴露于一个两个倍频程宽的短纯音组至少4个月,会降低初级听觉皮层(AI)对暴露频段内声音频率的反应性,并增加对该频段外边缘频率的反应性。在此,我们通过展示在68分贝声压级下6周暴露水平下定性相似的可塑性来扩展这一研究。尽管该暴露未诱发外周听力损失,但由此导致的AI音频拓扑图的重组类似于感觉上皮局限性损伤后的重组。从局部场电位的变化推断,大多数暴露引起的效应可能存在于丘脑,但在AI中进一步改变。然后,我们研究了在暴露停止后,在安静的实验室环境中恢复长达12周的情况下,这些变化逆转的可能性。虽然频率调谐恢复到接近正常水平,但在我们12周的观察期结束时,其他神经元反应特性以及音频拓扑图组织仍不正常。这可能对持续嘈杂的工作/娱乐/生活环境产生影响,即使在远低于目前认为不可接受的水平。