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Establishment of a Gentamicin Cochlear Poisoning Model in Guinea Pigs and Cochlear Nerve Endings Recognition of Ultrasound Signals
BACKGROUND: Aminoglycosides, a type of gram-negative antibacterial, are broad-spectrum antibiotics that are highly potent and have satisfactory therapeutic efficacy in the treatment of life-threatening infections. Our study aimed to establish a gentamicin-induced cochlear injury model and to investi...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scientific Literature, Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6322371/ https://www.ncbi.nlm.nih.gov/pubmed/30592260 http://dx.doi.org/10.12659/MSM.913205 |
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author | Wang, Fusen Gong, Shusheng Zhou, Yuee Huang, Chengcheng Li, Tiegang Li, Qian Ceng, Xinyu Wang, Chaoyan |
author_facet | Wang, Fusen Gong, Shusheng Zhou, Yuee Huang, Chengcheng Li, Tiegang Li, Qian Ceng, Xinyu Wang, Chaoyan |
author_sort | Wang, Fusen |
collection | PubMed |
description | BACKGROUND: Aminoglycosides, a type of gram-negative antibacterial, are broad-spectrum antibiotics that are highly potent and have satisfactory therapeutic efficacy in the treatment of life-threatening infections. Our study aimed to establish a gentamicin-induced cochlear injury model and to investigate the cochlear nerve endings’ recognition of ultrasound signals. MATERIAL/METHODS: A guinea pig cochlear injury model was established by intraperitoneal injection of gentamycin. Auditory brainstem response (ABR) and fMRI an affected cerebral cortex region of interest (ROI) of the cerebral cortex blood oxygenation level dependent (BOLD) effect was induced by bone-conducted ultrasound. Immunofluorescence was used to detect expression of Prestin in outer hair cells, Otoferlin in inner hair cells, and cochlear hair cell microfilament protein (F-Actin). RESULTS: For 30–35 KHz bone-conducted ultrasound, the induction rate of ABR threshold or ROI in the control group and the cochlear injury group was 40% and 0%, respectively, and for 80–90 KHz the induction rate was 20% and 20%, respectively. Gentamicin poisoning induced downregulation of expression of Prestin in cochlear outer cochlea, and Otoferlin and F-Actin in cochlear hair cells in different regions. CONCLUSIONS: Gentamicin poisoning can cause different degrees of damage to cochlea hair cells in different regions. Guinea pigs with gentamicin poisoning can recognize high-frequency ultrasonic signals. |
format | Online Article Text |
id | pubmed-6322371 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | International Scientific Literature, Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-63223712019-01-25 Establishment of a Gentamicin Cochlear Poisoning Model in Guinea Pigs and Cochlear Nerve Endings Recognition of Ultrasound Signals Wang, Fusen Gong, Shusheng Zhou, Yuee Huang, Chengcheng Li, Tiegang Li, Qian Ceng, Xinyu Wang, Chaoyan Med Sci Monit Animal Study BACKGROUND: Aminoglycosides, a type of gram-negative antibacterial, are broad-spectrum antibiotics that are highly potent and have satisfactory therapeutic efficacy in the treatment of life-threatening infections. Our study aimed to establish a gentamicin-induced cochlear injury model and to investigate the cochlear nerve endings’ recognition of ultrasound signals. MATERIAL/METHODS: A guinea pig cochlear injury model was established by intraperitoneal injection of gentamycin. Auditory brainstem response (ABR) and fMRI an affected cerebral cortex region of interest (ROI) of the cerebral cortex blood oxygenation level dependent (BOLD) effect was induced by bone-conducted ultrasound. Immunofluorescence was used to detect expression of Prestin in outer hair cells, Otoferlin in inner hair cells, and cochlear hair cell microfilament protein (F-Actin). RESULTS: For 30–35 KHz bone-conducted ultrasound, the induction rate of ABR threshold or ROI in the control group and the cochlear injury group was 40% and 0%, respectively, and for 80–90 KHz the induction rate was 20% and 20%, respectively. Gentamicin poisoning induced downregulation of expression of Prestin in cochlear outer cochlea, and Otoferlin and F-Actin in cochlear hair cells in different regions. CONCLUSIONS: Gentamicin poisoning can cause different degrees of damage to cochlea hair cells in different regions. Guinea pigs with gentamicin poisoning can recognize high-frequency ultrasonic signals. International Scientific Literature, Inc. 2018-12-28 /pmc/articles/PMC6322371/ /pubmed/30592260 http://dx.doi.org/10.12659/MSM.913205 Text en © Med Sci Monit, 2018 This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) ) |
spellingShingle | Animal Study Wang, Fusen Gong, Shusheng Zhou, Yuee Huang, Chengcheng Li, Tiegang Li, Qian Ceng, Xinyu Wang, Chaoyan Establishment of a Gentamicin Cochlear Poisoning Model in Guinea Pigs and Cochlear Nerve Endings Recognition of Ultrasound Signals |
title | Establishment of a Gentamicin Cochlear Poisoning Model in Guinea Pigs and Cochlear Nerve Endings Recognition of Ultrasound Signals |
title_full | Establishment of a Gentamicin Cochlear Poisoning Model in Guinea Pigs and Cochlear Nerve Endings Recognition of Ultrasound Signals |
title_fullStr | Establishment of a Gentamicin Cochlear Poisoning Model in Guinea Pigs and Cochlear Nerve Endings Recognition of Ultrasound Signals |
title_full_unstemmed | Establishment of a Gentamicin Cochlear Poisoning Model in Guinea Pigs and Cochlear Nerve Endings Recognition of Ultrasound Signals |
title_short | Establishment of a Gentamicin Cochlear Poisoning Model in Guinea Pigs and Cochlear Nerve Endings Recognition of Ultrasound Signals |
title_sort | establishment of a gentamicin cochlear poisoning model in guinea pigs and cochlear nerve endings recognition of ultrasound signals |
topic | Animal Study |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6322371/ https://www.ncbi.nlm.nih.gov/pubmed/30592260 http://dx.doi.org/10.12659/MSM.913205 |
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