FEATURE ARTICLE
The Design and Function of Cochlear Implants
Fusing medicine, neural science and engineering, these devices transform human speech into an electrical code that deafened ears can understand
Michael Dorman, Blake Wilson
Better Hearing Through Chemistry
In the near future, drug–delivery systems will be integrated
into the design of a cochlear implant. These systems will attempt to
do two things: arrest the shriveling or demise of remaining hair
cells and neural structures in the cochlea, and promote the growth
of neural tentacles called neurites from
spiral–ganglion cells toward the electrodes. If neurons in the
vicinity of each electrode can be kept alive, and especially if they
are brought closer to the electrodes with the growth of neurites,
then each electrode is more likely to function as an independent
channel of stimulation.
One approach is to inject growth–promoting neurotrophins into
the cochlea. In experiments with deafened guinea pigs, Takayuki
Shinohara and his coworkers at the Karolinska Institute in Stockholm
showed that by injecting brain–derived neurotrophic factor and
ciliary neurotrophic factor, they could increase the survival and,
critically, the sensitivity of spiral–ganglion cells. This
outcome hints at future implant designs in which neurites from
spiral ganglion cells grow toward multipurpose electrodes that
deliver electrical and pharmacological stimuli.
A second approach is to block apoptosis, the normal process
of cell death following injury. These self–destruct messages
can be triggered by many events, such as acoustic trauma or ototoxic
drugs, which work through a so–called mitogen–activated
protein kinase (MAPK) signaling pathway. The pathway can be blocked
at various points. One of the links in this chain is the protein
called c–Jun N–terminal kinase (JNK). This enzyme is the
target of a peptide inhibitor developed by a multi–center,
multi–national team that includes Jing Wang of the University
of Montpelier and Thomas Van De Water of the University of Miami. By
blocking JNK, they prevented hair–cell death and hearing loss
following acoustic trauma or administration of the ototoxic
antibiotic neomycin.
This outcome is especially relevant for future applications of
combined electric and acoustic stimulation. Injecting a
MAPK–JNK blocker could buffer existing hair cells from damage
caused by the surgery. In that case, the odds of preserving acoustic
hearing might increase, making combined EAS into a viable therapy
for a very large number of hearing–impaired people.
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