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Abstract
This study investigated the auditory behaviors of transgenic mice with deletions of
alpha9 nicotinic acetylcholine receptor subunits. In the normal mammalian cochlea,
the mechanical properties of outer hair cells are modified by the release of acetylcholine
from olivocochlear efferent terminals. Electrophysiological correlates of this efferent
feedback have not been demonstrated in alpha9 knockout mice, presumably because they
are mediated by alpha9 receptors. Previous studies have associated lesions of olivocochlear
pathways with hearing impairments in background noise. The prediction that alpha9
knockout mice would show similar deficits was tested by collecting psychophysical
thresholds for tone detection and intensity discrimination from knockout mice, within-strain
control subjects, and CBA/CaJ mice. Comparable performance was observed for the subject
groups in quiet and in continuous background noise. The preservation of auditory function
in alpha9 knockout mice suggests that central efferent pathways work in combination
with the peripheral olivocochlear system to enhance hearing in noise, and may compensate
for profound manipulations of peripheral feedback in highly routine testing procedures.
An intriguing possibility is that these central mechanisms include the brainstem collaterals
of olivocochlear neurons since their post-synaptic targets do not express alpha9 receptors
and therefore are likely to maintain their effects in alpha9 knockout mice.