This study investigated the auditory behaviors of transgenic mice with deletions of α9 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 α9 knockout mice, presumably because they are mediated by α9 receptors. Previous studies have associated lesions of olivocochlear pathways with hearing impairments in background noise. The prediction that α9 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 α9 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 α9 receptors and therefore are likely to maintain their effects in α9 knockout mice.
- Acetylcholine receptor knockout
- Auditory psychophysics
- Olivocochlear efferent feedback
ASJC Scopus subject areas
- Sensory Systems