Patrício M. V. Simões

This paper investigates how a Connexin 30 mutation affects cochlear electrophysiology, showing it rescues high-frequency hearing loss while impairing low-frequency hearing through changes in gap junction coupling and potassium currents in Deiters cells.

The paper uses optogenetics to study the role of supporting cells in force transmission to and from outer hair cells in the mouse cochlea, finding that hyperpolarizing these cells suppresses cochlear amplification and alters mechanical responses.

This study shows that a gap-junction mutation in mice preserves high-frequency hearing by maintaining extracellular receptor potentials in outer hair cells, suggesting these potentials drive cochlear amplification at high frequencies.