Can Cochlear Ion Transport Affect Cochlear Mechanics?

The potassium current circulating through the inner ear is instrumental in the mechanotransduction of auditory stimuli, allowing potassium ions (  to enter and depolarize hair cells, leading to neurotransmission and electromotility. To maintain homeostasis,  ions must return to the endolymph via cochlear marginal cells, which also help generate the endocochlear potential (EP). Our lab's computational models explore ion transport in the cochlea and its impact on hearing loss. Mutations in the I_sK current in marginal cells that increase channel conductance are linked to noise-induced hearing loss. We identified stable hypersensitive regions in transepithelial current profiles corresponding to elevated I_sK conductance. These regions correspond with regions where marginal cell swelling is predicted. Rreducing NKCC transporter activity (to simulate furosemide block) on the marginal cell’s basal side also creates hypersensitive regions. Experimentally, it has been shown that after the washout of furosemide, there is a lack of recovery of cochlear amplification compared to the EP.  This has been attributed to unknown processes that affect the cochlear amplifier's operating point (OP). We hypothesize that physical changes in marginal cells may operate by a similar indirect mechanism on cochlear mechanics.