Abstract:
:Potassium (K+) channels shape the response properties of neurons. Although enormous progress has been made to characterize K+ channels in the primary auditory neurons, the molecular identities of many of these channels and their contributions to hearing in vivo remain unknown. Using a combination of RNA sequencing and single molecule fluorescent in situ hybridization, we localized expression of transcripts encoding the sodium-activated potassium channels KNa1.1 (SLO2.2/Slack) and KNa1.2 (SLO2.1/Slick) to the primary auditory neurons (spiral ganglion neurons, SGNs). To examine the contribution of these channels to function of the SGNs in vivo, we measured auditory brainstem responses in KNa1.1/1.2 double knockout (DKO) mice. Although auditory brainstem response (wave I) thresholds were not altered, the amplitudes of suprathreshold responses were reduced in DKO mice. This reduction in amplitude occurred despite normal numbers and molecular architecture of the SGNs and their synapses with the inner hair cells. Patch clamp electrophysiology of SGNs isolated from DKO mice displayed altered membrane properties, including reduced action potential thresholds and amplitudes. These findings show that KNa1 channel activity is essential for normal cochlear function and suggest that early forms of hearing loss may result from physiological changes in the activity of the primary auditory neurons.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Reijntjes DOJ,Lee JH,Park S,Schubert NMA,van Tuinen M,Vijayakumar S,Jones TA,Jones SM,Gratton MA,Xia XM,Yamoah EN,Pyott SJdoi
10.1038/s41598-019-39119-zsubject
Has Abstractpub_date
2019-02-22 00:00:00pages
2573issue
1issn
2045-2322pii
10.1038/s41598-019-39119-zjournal_volume
9pub_type
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