Proteins may be required to grow auditory neurons

Loss of spiral ganglion neurons or hair cells in the inner ear is claimed to be a principal reason for congenital and acquired hearing impairment. Scientists from the University of California, San Diego, School of Medicine and the National Institutes of Health discovered that Sox2, a protein that controls stem cell formation, is said to be caught up in the growth of spiral ganglion neuron.

In the cochlea, auditory neurons supposedly send out sound vibrations delivered by hair cells. These vibrations are believed to be then changed to nerve impulses that seem to interact with the brain. Hearing loss arises, if the neurons are lost or destroyed. Current therapies for hearing loss are thought to be based on either augmenting hair cell stimulation by means of hearing aids or releasing an electronic alternative for the hair cells with cochlear implants. In either case, the attendance of efficient spiral ganglion neurons may be required for an effective outcome.

Alain Dabdoub, PhD, co-investigator and assistant professor of surgery with the division of otolaryngology at the UC San Diego School of Medicine, commented, “These findings may provide the first step toward regenerating spiral ganglion neurons, the nerve cells that send sound representations to the brain. This has significant implications for advances in cochlear implant technology and biological treatments for hearing loss.”

Preceding researches display that as less as 10 percent of the standard amount of spiral ganglion neurons may be adequate for the effectiveness of cochlear implants.

Chandrakala Puligilla, PhD, a research fellow at the National Institutes of Health, remarked, “The identification of factors that induce functional neurons has important implications for hearing restoration. The ability to induce even a small number of cells with gene-based therapy could be enormously beneficial.”

Sox2 is alleged to be a portion of the SoxB1 clan of proteins, which appears to play an important function in neural growth in the spinal cord and elsewhere. The research illustrates a new responsibility for Sox2 in ear development, displaying that Sox2 may be grave for the generation of auditory neurons and that spawning new neurons could be feasible.

Comprehending the molecular signaling pathways accountable for the growth of spiral ganglion neurons may be pertinent to other neurons, particularly those in the central nervous system.

The research was published in the Journal of Neuroscience.