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长期暴露于适度噪音会诱导幼鼠初级听觉皮层的神经可塑性。

Long-term exposure to moderate noise induces neural plasticity in the infant rat primary auditory cortex.

作者信息

Xia Chenchen, Yin Manli, Pan Ping, Fang Fanghao, Zhou You, Ji Yonghua

机构信息

Laboratory of Neuropharmacology and Neurotoxicology, Shanghai University, Shanghai, People's Republic of China.

Department of Otolaryngology-Head and Neck Surgery, Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People's Republic of China.

出版信息

Anim Cells Syst (Seoul). 2019 Jul 19;23(4):260-269. doi: 10.1080/19768354.2019.1643782. eCollection 2019.

DOI:10.1080/19768354.2019.1643782
PMID:31489247
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6711034/
Abstract

Previous studies have reported that rearing infant rat pups in continuous moderate-level noise delayed the formation of topographic representational order and the refinement of response selectivity in the primary auditory (A1) cortex. The present study further verified that exposure to long-term moderate-intensity white noise (70 dB sound pressure level) from postnatal day (P) 12 to P30 elevated the hearing thresholds of infant rats. Compared with age-matched control rats, noise exposure (NE) rats had elevated hearing thresholds ranging from low to high frequencies, accompanied by decreased amplitudes and increased latencies of the two initial auditory brainstem response waves. The power of raw local field potential oscillations and high-frequency oscillation in the A1 cortex of NE rats were larger, whereas the power of high-frequency oscillation was smaller than that of control rats. In addition, the expression levels of five glutamate receptor (GluR) subunits in the A1 cortex of NE rats were decreased with laminar specificity. These results suggest that the altered neural excitability and decreased GluR expression may underlie the delay of functional maturation in the A1 cortex, and may have implications for the treatment of hearing impairment induced by environmental noise.

摘要

先前的研究报道,将新生幼鼠饲养在持续的中等强度噪音环境中会延迟初级听觉(A1)皮层中地形表征顺序的形成以及反应选择性的精细化。本研究进一步证实,从出生后第(P)12天到P30天暴露于长期中等强度白噪声(声压级70 dB)会提高幼鼠的听力阈值。与年龄匹配的对照大鼠相比,噪声暴露(NE)大鼠从低频到高频的听力阈值均升高,同时最初两个听觉脑干反应波的振幅降低、潜伏期延长。NE大鼠A1皮层中原始局部场电位振荡和高频振荡的功率更大,而高频振荡的功率比对照大鼠小。此外,NE大鼠A1皮层中五个谷氨酸受体(GluR)亚基的表达水平具有层特异性降低。这些结果表明,神经兴奋性改变和GluR表达降低可能是A1皮层功能成熟延迟的基础,并且可能对环境噪声引起的听力损伤的治疗具有启示意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7401/6711034/f617a3265bae/TACS_A_1643782_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7401/6711034/1be1c6a8b391/TACS_A_1643782_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7401/6711034/39c3ebb2ff9b/TACS_A_1643782_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7401/6711034/d2d23e6c7f72/TACS_A_1643782_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7401/6711034/f617a3265bae/TACS_A_1643782_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7401/6711034/1be1c6a8b391/TACS_A_1643782_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7401/6711034/39c3ebb2ff9b/TACS_A_1643782_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7401/6711034/d2d23e6c7f72/TACS_A_1643782_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7401/6711034/f617a3265bae/TACS_A_1643782_F0004_OC.jpg

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