Volume 8 Issue 1 (pdf) - Andrew John Publishing Inc

esearCh and deVeLoPMent foCus |
Early Age Conductive Hearing Loss Impairs
Sound Tolerance and Auditory Processing
By Wei Sun, PhD, yuguang Niu, Senthilvelan Manohar, Anand Kumaraguru and Brian Allman, PhD
Otitis media is a common illness
diagnosed in children. Chronic
otitis media at early age, especially in
infants, can induce recurrent conductive
hearing loss which may adversely affect
language acquisition, learning and social
interactions. 1 Recent clinical studies
have found that children who reported
hearing loss often experienced
hyperacusis and tinnitus (~37%),
suggesting that mild hearing loss during
early age might be an associated risk
factor for hyperacusis and tinnitus in
children. 2 Given that sensory input from
the cochlea is crucial for the functional
development of the central auditory
system, 3,4 we hypothesized that early age
hearing loss would affect the normal
development of the central auditory
system and disrupt sound perception
and tolerance. In the present study, we
tested this hypothesis using Sprague
Dawley rats as an animal model.
During light anesthesia, we surgically
perforated the tympanic membranes of
rats at postnatal 16 days (note that a rat’s
ear canals do not open until postnatal
About the Author
Wei Sun (pictured) is with the Center for Hearing &
Deafness, Department of Communicative Disorders
and Sciences, the State University of New York at
Buffalo, Buffalo, NY.
12 days). After surgery, the rats
developed a temporary conductive
hearing loss for about 2–3 weeks until
the trauma of the ear drum had healed.
Surprisingly, several weeks after the
tympanic membrane perforation, more
than 85% of the rats (n = 23) developed
a susceptibility to audiogenic seizure,
which was characterized by wild
running followed by erratic leaping and
clonic convulsion during exposure to
loud sound (120 dB SPL white noise,
< 1 minute. The susceptibility of
audiogenic seizure lasted to adulthood;
long after hearing loss had recovered.
Furthermore, compared to age-matched
controls, rats with early age tympanic
membrane damage also showed
enhanced acoustic startle responses.
These results suggest that early age
hearing loss can increase sound
sensitivity and reduce sound tolerance.
By varying the timing of the tympanic
membrane surgery, we found that
audiogenic seizures could also be
induced when tympanic membrane
perforation occurred at postnatal 30
days, but not at postnatal 45 days;
findings which suggest that hearing loss
in early life results in a greater
impairment of sound perception and
tolerance than hearing loss in
adulthood.
We further evaluated the changes in
auditory processing induced by early
age conductive hearing loss by
comparing, within a given animal, the
auditory brainstem responses (ABRs)
evoked during sound presentation to
the tympanic membrane damaged ear
versus undamaged (control) ear.
Although the ABR threshold showed no
significant difference between the
control ears versus the tympanic
membrane damaged ears two months
after the surgery, the ABR interwave
latencies of waves of I to V in the
tympanic membrane damaged ears were
significantly shorter than the ears
without tympanic membrane damage.
In addition, using immunostaining for
c-Fos, an immediate gene whose
activation can be used to indicate neural
activity, we found a stronger staining in
the inferior colliculus in the tympanic
membrane damaged rats after exposure
to loud sound compared to the rats
without tympanic membrane damage.
These results suggest that early age
hearing loss may cause hyperexcitability
and increase the neural signal
conduction in the central auditory
system.
In a follow-up series of experiments, we
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