Inhibition of connexin 43 induces hearing loss in postnatal mice

Abstract

BackgroundConnexin 43 (Cx43) is the most ubiquitously expressed member of the family of connexins, constituting gap junctions and mediating cell communication, still its role in hearing loss has been little studied.MethodsImmunohistochemistry was used to detect the expression pattern of Cx43. Spiral ganglia neurons (SGNs) and Corti co-culture were utilized to assay the re-innervation of hair cells by newborn SGNs. Gap19 was utilized to inhibit Cx43 hemichannels. Auditory brainstem responses (ABR) and endocochlear potential (E.P.) were measured to confirm the hearing loss.ResultsThe expression of Cx43 in P14 mice was higher than in P0 and P28 (adult) mice, the earlier time point coinciding with the early inner ear development. Additionally, the growth and synapse generation of fibers were inhibited after Gap 19 treatment of the co-cultures of the Corti and SGNs from newborn mice. Furthermore, the inhibition of Cx43 could increase the ABR threshold and decrease E.P. level in postnatal mice, whereas such an effect was not observed in adult mice.ConclusionThe function of Cx43 is critical during the early development of mouse cochlea but is dispensable in adult mice.

MiR-106a facilitates the sensorineural hearing loss induced by oxidative stress by targeting connexin-43

“…Connexin 43, a member of the connexins family, belongs to type II connexin, which is the first connexin that is confirmed associated with deafness [ 14 ]. Zhang reported that the mild hearing loss could be induced by the downregulation of connexin 43 [ 48 ], which was supported by Wang [ 49 ] using a postnatal mice model. We found that the declined expression level of connexin 43 was both observed in GO-treated MCs and cochlear tissues of SNHL rats, suggesting connexin 43 might be protective to the development of SNHL.…”