Scientists restored hearing to mice that were partly deafened by noise. They did it by increasing a key protein in their ears.
The protein, called NT3, is critical for maintaining communication between the ears and brain.
The work, reported in the journal eLife, suggests the protein might be a target for treating people who have suffered hearing loss due to noise or aging.
In addition to the protein, the study also looked at the role of cells that have traditionally been seen as the “supporting actors” of the ear-brain connection.
Called supporting cells, they form a physical base for the hearing system’s “stars”: the hair cells in the ear that interact directly with the nerves that carry sound signals to the brain. This new research identifies the critical role of these supporting cells along with the NT3 molecules that they produce.
NT3 is crucial to the body’s ability to form and maintain connections between hair cells and nerve cells, the researchers demonstrate. This special type of connection, called a ribbon synapse, allows extra-rapid communication of signals that travel back and forth across tiny gaps between the two types of cells.
“It has become apparent that hearing loss due to damaged ribbon synapses is a very common and challenging problem, whether it’s due to noise or normal aging,” says Gabriel Corfas, who led the team and directs the University of Michigan Medical School’s Kresge Hearing Research Institute.
“We began this work 15 years ago to answer very basic questions about the inner ear, and now we have been able to restore hearing after partial deafening with noise, a common problem for people. It’s very exciting.”
A therapy for people?
Using a special genetic technique, the researchers made it possible for some mice to produce additional NT3 in cells of specific areas of the inner ear after they were exposed to noise loud enough to reduce hearing. Mice with extra NT3 regained their ability to hear much better than the control mice.
Now, says Corfas, his team will explore the role of NT3 in human ears, and seek drugs that might boost NT3 action or production. While the use of such drugs in humans could be several years away, the new discovery gives them a specific target to pursue.
Boosting NT3 production through gene therapy in humans could also be an option, he says, but a drug-based approach would be simpler and could be administered as long as it takes to restore hearing.
Corfas notes that the mice in the study were not completely deafened, so it’s not yet known if boosting NT3 activity could restore hearing that has been entirely lost. He also notes that the research may have implications for neurodegenerative diseases.
Researcher from Harvard University collaborated on the project, which was funded by the National Institute on Deafness and Other Communication Disorders, the Eunice Kennedy Shriver National Institute of Child Health and Human Development, and the Hearing Health Foundation.
Source: University of Michigan