Hearing loss is believed to originate in non-sensory cells in the cochlea, the auditory portion of the inner ear containing the organ which produces nerve impulses in response to sound.
The cells are coupled together by ‘gap junctions’ which are formed of two proteins called connexin 26 and connexin 30. It is mutations or failures in these proteins that cause most cases of hearing loss.
However, experiments by the university’s Sensory Neuroscience Research Group have shown that one particular mutation in the connexion 30 protein actually prevents deafness to high-frequency sound.
Professor Ian Russell, the University of Brighton’s Professor of Neurobiology and a member of the group, said: “This was a great surprise: The mutation should have impaired the function of the cochlea, not aided it.”
He said: “Other members of the research team are now making direct measurements from these supporting cells to understand how the mutation changes the properties of the gap junctions. They should obtain measurements that will enable us to understand how the mutation alters the electrical and mechanical properties of the cochlea and eventually lead to our understanding how sensitivity is preserved in a cochlea that would otherwise be decimated by age-related-hearing-loss.”