First Step in Improving Function of Cochlear Implants through Biological Process

From: Newswise (press release) - USA - Feb 21, 2004

Newswise — Since the first cochlear implants were inserted in the late 1970's, they have revolutionized treatment for the nearly 23,000 severely hearing impaired Americans who have received the devices. Science has yet to mimic the complex mechanism of the human ear as it responds to sound, or compensate for the natural differences of the human body, but researchers in the US and Germany are working together to improve the function of cochlear implants using the body's own cells.

A cochlear implant is an electronic device designed for people with severe to profound hearing loss who can derive little or no benefit from hearing aids. The device cannot restore hearing; it allows the user to hear sounds, which must then be interpreted into speech. The cochlear implant consists of a sound processor with electrodes that are surgically attached to the cochlea (part of the inner ear). When turned on, the sound processor translates sound into electrical signals, which are transferred to electrodes that stimulate the hearing nerve, which sends information to the brain so it can interpret sound. In recent years, technological advancements in cochlear implants have expanded the number of information channels available to about ten, a vast improvement in the ability to translate sound. However, compare those ten channels to the thousands of channels a normal hearing cochlea uses and the limitations of current technology becomes clear.

Based on the knowledge that more information channels will increase the effectiveness of cochlear implants, researchers have set out to develop a biological strategy to entice spiral ganglion neurons and dendrites (tiny parts of the hearing nerve system) to grow very close to the electrodes of a cochlear implant. If successful, this strategy might allow the body's own cells to create hundreds of information channels, dramatically improving the function of cochlear implants.

The first step of this effort, a study with animal cells, was undertaken by Allen Ryan, and Lina Mullen, Kwang Pak, and John Wittig, Joanna Xie, of the University of California San Diego School of Medicine in La Jolla, Dominik Brors and Christof Aletsee of the University of Wurzburg, and Stefan Dazert of Ruhr-University Bochum, Germany. The results of their work, "Regrowth of Spiral Ganglion Neurites to a Cochlear Implant," will be presented at the Mid Winter Meeting of the Association for Research in Otolaryngology (www.aro.org) being held February 22-26, 2004 at the Adam's Mark Hotel, Daytona Beach, FL.

Methodology: Spiral ganglion (SG) explants (each containing 50 to 100 neurons) were dissected from rodents and allowed to grow in various mediums; some including growth factors. Neurites were measured throughout the study by computer analysis to determine length, degree, and direction of growth. Various forms of statistical analysis were used to analyze the resulting data. The following were investigated:
a. The effects of growth factors on neurite extension from SG explants.
b. The role of extracellular matrix molecules in SG neuritis extension.
c. Eph/ephrin signaling (a large class of cell proteins whose signaling plays an important role in neurite pathfinding in the brain).
d. Growth of SG neurites in three-dimensional cultures. (Neurites need a structure on which to grow.)
e. Microchambers for evaluation of neurite responses to competing signals.
f. Interaction of SG neurites with hair cells of the inner ear.
g. Response of SG neurites to cochlear implant materials.

Results: The concentration level of a variety of growth factors was found to be key in the successful enhancement of neurite growth. Certain extracellular matrices increased neurite length and some induced a turn in direction of growth, but the number of neurites was not affected by the matrices. Eph/ephrin signaling provides directional input to SG neurites through negative influence. SG neurites prefer a structure on which they can grow; a collagen gel was successful in providing a suitable growth structure. Channel networks (microchambers) proved successful at directing SG neurites toward a particular target. SG neurites were shown to grow toward inner ear hair cells and make contact with them. Interestingly, it was found that the materials and design of a cochlear implant could be used to influence neurite growth. Specifically, titanium strongly encouraged growth of neurites, which were more likely to form on electrodes mounted flush to the implant.

Conclusion: This study provides evidence that targeted (toward the cochlear implant) regrowth of spiral ganglion cells in the inner ear may be possible; representing the first step in determining whether the body's own growth mechanisms can be enlisted to improve cochlear implant functionality. These results may also influence future material and design of cochlear implants. Further investigation is needed to define how spiral ganglion regrowth might be best achieved and the extent of benefit from this strategy.

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