NEW BRUNSWICK, N.J. – A Rutgers University team led by neuroscientist Robin Davis is opening new doors to improved hearing for the congenitally or profoundly deaf. Their findings could lead to a new generation of cochlear implants.
Cochlear implants today operate with varying degrees of success in different patients. Some may be able to hear sounds like the rush of traffic or the crash of thunder. Others can do even better, detecting voice and understanding speech while still being unable to appreciate music. With the latest research, across-the-board improvement may be within reach.
Davis’ work is important for engineers and surgeons in designing new cochlear implants. “The significance of our work lies in the fact that we can change an element in a very peripheral part of the sensory system that can have an impact all the way into the brain,” Davis said.
Cochlear implants, also known as “bionic ears,” are surgically inserted into the snail-shell shaped structure – the cochlea – within the inner ear. Ordinarily, hair cells line the cochlea and convert acoustic signals into electrical signals that nerves then carry to the brain. Where some hair cells exist, sounds can be amplified with a hearing aid. Where the hair cells are missing or damaged – a condition generally associated with severe hearing impairment – an implant may be used to replace their function.
Davis, a professor in the Department of Cell Biology and Neuroscience of Rutgers’ School of Arts and Sciences, works with mouse cochlear tissue cultured in the laboratory. The spiraled cochlea is unwound and laid out in a line. Davis described the hair cells as being analogous to the keys of a piano and the nerves to which they attach – the spiral ganglion neurons that connect to the brain – are the piano’s strings.
“Our studies have revealed that spiral ganglion auditory neurons possess a rich complexity that is only now beginning to be understood,” said Davis.
The researchers found that two neurotrophin proteins in the cochlea – brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) – figure prominently in the relay of sound messages to the brain. Research by Davis and her team, begun more than six years ago, is now producing insights into precisely how these multidimensional proteins operate in the cochlea. These most recent findings appear in the Dec. 19 issue of The Journal of Neuroscience.
While neurotrophins have historically been prized for the survival value they impart to nerve cells, the researchers found that in the cochlea they do a great deal more. Their presence in relative proportions transforms the spiral ganglion neurons into either fast-firing transmitters to carry high pitched sound messages to the brain, or slow-firing carriers for the transmission of lower pitched signals. The neurotrophins accomplish this at the molecular level by tightly regulating a newly-defined and complex series of signaling proteins.
Davis explained that one end of the cochlea is home to the slower-firing neurons characterized by a preponderance of NT-3, while the other cochlear end is rich in BDNF, making those neurons faster-firing. Both neurotrophins are present in gradients throughout the range, but at any specific locale their amounts vary relative to each other – lots of BDNF and a little NT-3 in the high frequency transmitters, for example, and the reverse as you move toward the other end.
In one possible remedial approach, Davis described how the neurotrophins could potentially be pumped into a newly-designed cochlear implant and released through graduated ports along its length.