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Neural Plasticity
Volume 2016, Article ID 4545826, 10 pages
Research Article

Synchronized Progression of Prestin Expression and Auditory Brainstem Response during Postnatal Development in Rats

1Department of Physiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China
2Department of Laboratory Medicines, General Hospital of Guangzhou Military Command of PLA, Guangzhou 510010, China
3Affiliated High School of South China Normal University, Guangzhou 510630, China

Received 8 September 2016; Revised 8 November 2016; Accepted 30 November 2016

Academic Editor: Jian Wang

Copyright © 2016 Jianfeng Hang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Prestin is the motor protein expressed in the cochlear outer hair cells (OHCs) of mammalian inner ear. The electromotility of OHCs driven by prestin is responsible for the cochlear amplification which is required for normal hearing in adult animals. Postnatal expression of prestin and activity of OHCs may contribute to the maturation of hearing in rodents. However, the temporal and spatial expression of prestin in cochlea during the development is not well characterized. In the present study, we examined the expression and function of prestin from the OHCs in apical, middle, and basal turns of the cochleae of postnatal rats. Prestin first appeared at postnatal day 6 (P6) for basal turn, P7 in middle turn, and P9 for apical turn of cochlea. The expression level increased progressively over the next few days and by P14 reached the mature level for all three segments. By comparison with the time course of the development of auditory brainstem response for different frequencies, our data reveal that prestin expression synchronized with the hearing development. The present study suggests that the onset time of hearing may require the expression of prestin and is determined by the mature function of OHCs.