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Expression and localization of α(2A)-adrenergic receptor in the rat post-natal developing cochlea

Lots of adrenergic receptors (ARs) are widely present across the auditory pathways and are positioned to affect auditory and vestibular functions. However, noradrenergic regulation in the cochlea has not been well characterized. In this study, a rat model of noise-induced hearing loss was developed...

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Detalles Bibliográficos
Autores principales: Tian, Chaoyong, Yang, Yang, Li, Yao, Sun, Fei, Qu, Juan, Zha, Dingjun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: PAGEPress Publications, Pavia, Italy 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10476538/
https://www.ncbi.nlm.nih.gov/pubmed/37548252
http://dx.doi.org/10.4081/ejh.2023.3748
Descripción
Sumario:Lots of adrenergic receptors (ARs) are widely present across the auditory pathways and are positioned to affect auditory and vestibular functions. However, noradrenergic regulation in the cochlea has not been well characterized. In this study, a rat model of noise-induced hearing loss was developed to investigate the expression of α(2A)-adrenergic receptor (AR) after acoustic trauma, then, we investigated the expression of α(2A)-AR in the developing rat cochlea using immunofluorescence, qRT-PCR, and Western blotting. We found that the expression of α(2A)-AR significantly increased in rats exposed to noise compared with controls. Immunofluorescence analysis demonstrated that α(2A)-AR is localized on hair cells (HCs), spiral ganglion neurons (SGNs), and the stria vascularis (SV) in the postnatal developing cochlea from the post-natal day (P) 0 to P28. Furthermore, we observed α(2A)-AR mRNA reached a maximum level at P14 and P28 when compared with P0, while no significant differences in α2A-AR protein levels at the various stages when compared with P0. This study provides direct evidence for the expression of α2A-AR in HCs, SGNs, and the SV of the cochlea, indicating that norepinephrine might play a vital role in hearing function within the cochlea through α2A-AR.