Spotlight on Spiral Ganglion Cells— New Research in Regeneration

Alain Dabdoub, Ph.D., University of California School of Medicine, San Diego (organizer); Robin Davis, Ph.D., Rutgers University; Albert Edge, Ph.D., Harvard Medical School, Massachusetts Eye and Ear Infirmary; Bernd Fritzsch, Ph.D., University of Iowa (among the presenters)

Spiral ganglion neurons (SGNs) transmit sound information in the form of electrical signals from the sensory cells in the inner ear, called hair cells, to the cochlear nucleus of the brainstem. Once lost due to noise or aging, SGNs and hair cells in mammals are never recovered. The most common therapies for hearing loss either use hearing aids to increase hair cell stimulation or use cochlear implants as an electronic substitute for damaged hair cells, but both therapies depend on the presence of functional SGNs. However, recent evidence shows that exposure to loud noise over time can lead to hearing loss caused not by damage to hair cells, but by loss of SGNs, and interest is rising in looking at strategies for replacing damaged or missing SGNs in the cochlea. This symposium features presentations from some of the most prominent investigators in the field of SGN regeneration, whose findings could play a significant role in future advances in cochlear implant technology and the medical treatment of hearing loss and deafness. Dr. Bernd Fritzsch will share findings from his laboratory, where they are elucidating the molecular mechanisms that regulate hair cell and SGN formation, particularly the factors that appear to regulate the growth and guidance of SGN fibers. Dr. Robin Davis will describe the diversity of organization, protein expression, and electrophysiological characteristics of neurons in the SGN family—not all SGNs are alike. Dr. Albert Edge will discuss his laboratory's efforts to generate SGNs using mouse embryonic stem cells and to reconnect healthy hair cells to the stem cell-derived neurons. Dr. Dabdoub will also be discussing how he and his colleagues are working to reprogram cochlear non-sensory epithelial cells to become functional SGNs.