AUTHOR=Lv Jun , Fu Xiaolong , Li Yige , Hong Guodong , Li Peipei , Lin Jing , Xun Youfang , Fang Lucheng , Weng Weibin , Yue Rongyu , Li Geng-Lin , Guan Bing , Li He , Huang Yideng , Chai Renjie 

TITLE=Deletion of Kcnj16 in Mice Does Not Alter Auditory Function

JOURNAL=Frontiers in Cell and Developmental Biology

VOLUME=9

YEAR=2021

URL=https://www.frontiersin.org/journals/cell-and-developmental-biology/articles/10.3389/fcell.2021.630361

DOI=10.3389/fcell.2021.630361

ISSN=2296-634X

ABSTRACT=<p>Endolymphatic potential (EP) is the main driving force behind the sensory transduction of hearing, and K<sup>+</sup> is the main charge carrier. Kir5.1 is a K<sup>+</sup> transporter that plays a significant role in maintaining EP homeostasis, but the expression pattern and role of Kir5.1 (which is encoded by the <italic>Kcnj16</italic> gene) in the mouse auditory system has remained unclear. In this study, we found that Kir5.1 was expressed in the mouse cochlea. We checked the inner ear morphology and measured auditory function in <italic>Kcnj16</italic><sup>–/–</sup> mice and found that loss of <italic>Kcnj16</italic> did not appear to affect the development of hair cells. There was no significant difference in auditory function between <italic>Kcnj16</italic><sup>–/–</sup> mice and wild-type littermates, although the expression of <italic>Kcnma1</italic>, <italic>Kcnq4</italic>, and <italic>Kcne1</italic> were significantly decreased in the <italic>Kcnj16</italic><sup>–/–</sup> mice. Additionally, no significant differences were found in the number or distribution of ribbon synapses between the <italic>Kcnj16</italic><sup>–/–</sup> and wild-type mice. In summary, our results suggest that the <italic>Kcnj16</italic> gene is not essential for auditory function in mice.</p>