Ning Zhao1,2, XuHui Tai3, LiJie Zhai4, Lin Shi4, DaiShi Chen5,6, Bo Yang1, Fei Ji6, Kun Hou6, ShiMing Yang6, ShuSheng Gong2, Ke Liu2. 1. a Department of Otolaryngology-Head and Neck Surgery , The First Affiliated Hospital of China Medical University , Shenyang , China. 2. b Department of Otolaryngology, Head and Neck Surgery , Beijing Friendship Hospital, Capital Medical University , Beijing , China. 3. c Department of Otolaryngology , The No 463rd Hospital of PLA , Shenyang , China. 4. d Department of Otolaryngology-Head and Neck Surgery , The First Affiliated Hospital of DaLian Medical Universty , Dalian , China. 5. e Department of Neurosurgery , Medical Faculty of the Friedrich Alexander University of Erlangen-Numberg (FAU) , Erlangen , Germany. 6. f Department of Otolaryngology-Head and Neck Surgery , General Hospital of PLA and the E.N.T Institute of PLA , Beijing , China.
Abstract
BACKGROUND: Previous study showed that mild ototoxic exposure could induce a reversible hearing impairment, and the loss and secondary incomplete recovery of cochlear ribbon synapses could be responsible for the hearing loss. However, it remains unclear whether cochlear outer hair cells' (OHCs) functions are affected. OBJECTIVE: To verify whether the function of OHCs are also affected significantly after the ototoxic exposure. METHODS: Mice were injected intraperitoneally with 100 mg/kg concentration of gentamicin daily for 14 days. Distortion Product of Oto-acoustic Emission (DPOAE) was detected at control (pre-treatment), Day 0, day 4, day 7, day 14 and day 28 after the ototoxic exposure, respectively. In addition, the morphology of OHCs was observed by electron microscopy, OHCs has been counted by light microscopy, and the hearing thresholds were detected by auditory brain response (ABR). RESULTS: No significant changes have been found in OHC and OHC stereocilia among the experimental groups (p > .05). Further, no significant changes or loss was found in the morphology of OHCs either. However, we found ABR threshold elevations occurred after ototoxic exposure. CONCLUSIONS: Unitary ototoxic gentamicin exposure may not disrupt the function of cochlear OHCs in mice, regardless of hearing loss identified in this ototoxic exposure.
BACKGROUND: Previous study showed that mild ototoxic exposure could induce a reversible hearing impairment, and the loss and secondary incomplete recovery of cochlear ribbon synapses could be responsible for the hearing loss. However, it remains unclear whether cochlear outer hair cells' (OHCs) functions are affected. OBJECTIVE: To verify whether the function of OHCs are also affected significantly after the ototoxic exposure. METHODS:Mice were injected intraperitoneally with 100 mg/kg concentration of gentamicin daily for 14 days. Distortion Product of Oto-acoustic Emission (DPOAE) was detected at control (pre-treatment), Day 0, day 4, day 7, day 14 and day 28 after the ototoxic exposure, respectively. In addition, the morphology of OHCs was observed by electron microscopy, OHCs has been counted by light microscopy, and the hearing thresholds were detected by auditory brain response (ABR). RESULTS: No significant changes have been found in OHC and OHC stereocilia among the experimental groups (p > .05). Further, no significant changes or loss was found in the morphology of OHCs either. However, we found ABR threshold elevations occurred after ototoxic exposure. CONCLUSIONS: Unitary ototoxicgentamicin exposure may not disrupt the function of cochlear OHCs in mice, regardless of hearing loss identified in this ototoxic exposure.