• Haixia Hu, Yan Ma, Bin Ye, Quan Wang, Tao Yang, Jingrong Lv, Jun Shi, Hao Wu, and Mingliang Xiang.
• Department of Otolaryngology & Head and Neck Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, China; Ear Institute, Shanghai Jiaotong University School of Medicine, Shanghai 200092, China; Shanghai Key Laboratory of Translational Medicine on Ear and Nose Diseases, Shanghai 200092, China.
• Neuroscience. 2017 Jan 26; 341: 1-8.

AbstractEfr3a has been found to be involved in the functional maintenance and structural degeneration of sensory and motor nervous tissues. Our previous data have suggested that Efr3a may be associated with the initiation of the degeneration of spiral ganglion neurons (SGNs). In this study, we used Efr3a knockdown (Efr3a KD) and Efr3a overexpression (Efr3a OE) mice to determine the role of Efr3a in age-related hearing loss. Measurements of hearing thresholds showed that Efr3a had little or no influence on the hearing threshold at all frequencies in adult mice, whereas in an early stage of senescence, Efr3a reduction resulted in better hearing function, especially at 10 and 12months of age. No significant differences were observed in hair cell loss among the three groups until 14months. The number of surviving hair cells in the OE mice was lower than that in the KD mice. As indicated by the density of SGNs in the upper basal turn, the Efr3a OE mice displayed earlier and more severe degeneration than the KD mice. In addition, the p-Akt levels in the cochlear spiral ganglions were higher in adult Efr3a KD mice than in WT and OE mice, although there was no difference in Akt expression among the three groups. Our study suggests that down-regulation of Efr3a might improve hearing function and alleviate the degeneration of SGNs in an early stage of senescence, probably via enhancing the basal expression of activated Akt.Copyright © 2016 IBRO. Published by Elsevier Ltd. All rights reserved.

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