Tao Shan, Liu Lijie, Shi Lijuan, Li Xiaowei, Shen Pei, Xun Qingying, Guo Xiaojing, Yu Zhiping, Wang Jian
Department of Physiology, Medical College of Southeast University, Nanjing, China.
Children's Medical Center, the Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
J Otol. 2015 Mar;10(1):21-28. doi: 10.1016/j.joto.2015.07.001. Epub 2015 Aug 8.
Noise pollution is a major hazardous factor to human health and is likely harmful for vulnerable groups such as pre-term infants under life-support system in an intensive care unit. Previous studies have suggested that noise exposure impairs children's learning ability and cognitive performance and cognitive functions in animal models in which the effect is mainly attributed to the oxidant stress of noise on the cognitive brain. The potential role of noise induced hearing loss (NIHL), rather than the oxidant stress, has also been indicated by a depression of neurogenesis in the hippocampus long after a brief noise exposure, which produces only a tentative oxidant stress. It is not clear if noise exposure and NIHL during early development exerts a long term impact on cognitive function and neurogenesis towards adulthood. In the present study, a brief noise exposure at high sound level was performed in neonatal C57BL/6J mice (15 days after birth) to produce a significant amount of permanent hearing loss as proved 2 months after the noise. At this age, the noise-exposed animals showed deteriorated spatial learning and memory abilities and a reduction of hippocampal neurogenesis as compared with the control. The averaged hearing threshold was found to be strongly correlated with the scores for spatial learning and memory. We consider the effects observed are largely due to the loss of hearing sensitivity, rather than the oxidant stress, due to the long interval between noise exposure and the observations.
噪音污染是对人类健康的一个主要危险因素，对诸如重症监护病房中依靠生命支持系统的早产儿等弱势群体可能有害。先前的研究表明，噪音暴露会损害儿童的学习能力以及认知表现，并且在动物模型中会损害认知功能，其影响主要归因于噪音对大脑认知区域的氧化应激。短暂噪音暴露后很长时间，海马体神经发生受到抑制，这也表明了噪音性听力损失（NIHL）而非氧化应激的潜在作用，短暂噪音暴露只会产生暂时的氧化应激。尚不清楚早期发育过程中的噪音暴露和NIHL是否会对成年期的认知功能和神经发生产生长期影响。在本研究中，对新生C57BL/6J小鼠（出生后15天）进行了一次高声级短暂噪音暴露，结果显示噪音暴露2个月后出现了大量永久性听力损失。在这个年龄，与对照组相比，噪音暴露组动物的空间学习和记忆能力下降，海马体神经发生减少。平均听力阈值与空间学习和记忆得分密切相关。我们认为观察到的这些影响很大程度上是由于听力敏感性丧失，而非氧化应激，因为噪音暴露与观察之间间隔时间较长。
