Deletion of Kcnj16 in Mice Does Not Alter Auditory Function

Abstract

Endolymphatic potential (EP) is the main driving force behind the sensory transduction of hearing, and K⁺ is the main charge carrier. Kir5.1 is a K⁺ transporter that plays a significant role in maintaining EP homeostasis, but the expression pattern and role of Kir5.1 (which is encoded by the <i>Kcnj16</i> 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 <i>Kcnj16</i> ^-/- mice and found that loss of <i>Kcnj16</i> did not appear to affect the development of hair cells. There was no significant difference in auditory function between <i>Kcnj16</i> ^-/- mice and wild-type littermates, although the expression of <i>Kcnma1</i>, <i>Kcnq4</i>, and <i>Kcne1</i> were significantly decreased in the <i>Kcnj16</i> ^-/- mice. Additionally, no significant differences were found in the number or distribution of ribbon synapses between the <i>Kcnj16</i> ^-/- and wild-type mice. In summary, our results suggest that the <i>Kcnj16</i> gene is not essential for auditory function in mice.