Hearing Better: Mice Restored From Partial Deafness

By manipulating the expression of certain nerve cell growth factors in mice, a collaborative team between the University of Michigan Medical School and Harvard University […]

By manipulating the expression of certain nerve cell growth factors in mice, a collaborative team between the University of Michigan Medical School and Harvard University has yielded results indicating that partial deafness can be counteracted. Studies of neurotrophin-3 (Ntf3) and brain-derived neurotrophic factor (Bdnf), two key decision-making proteins in developing and mature nerve cells, led to the elucidation of the mechanisms through which these factors maintain a communicative network between the auditory neurons and the brain.

A neurotrophin is a small, secreted protein, akin to a hormone, that regulates the growth and survival of developing neurons, which intrigued these researchers, who are affiliated with the Kresge Hearing Research Institute. The involvement of Ntf3 and Bdnf in embryonic aural neuron proliferation has been well documented, but little was known about their potential postnatal functions. Designing inducible knockout and over-expression methods to alter the cellular presence of these growth factors allowed the researchers to see that the expression of Ntf3 and Bdnf are essential for the formation of ribbon synapses, the degradation of which is linked with loss of hearing in both mice and humans.

The scientists subjected mice to noises loud enough to create synaptopathy (the dysfunction of synapses) between cochlear nerves and hair cells, the auditory sensory receptors in vertebrates. Then, with an overexpression of Ntf3, the mice were able to regenerate these synapses, and thereby recover their hearing. These results have widespread relevance, as auditory synaptopathy is a primary cause of hearing loss associated with noise, and this study presents a potential therapeutic solution.

Furthermore, other diseases such as autism, Alzheimer’s, and schizophrenia are also associated with synaptopathy, and this study suggests novel methods for tackling those diseases.

About Jacob Verter