Long-term sound conditioning enhances cochlear sensitivity

Sound conditioning, by chronic exposure to moderate-level sound, can protec t the inner ear (reduce threshold shifts and hair cell damage) from subsequ ent high-level sound exposure. To investigate the mechanisms underlying thi s protective effect, the present study focuses on the physiological changes brought on by the conditioning exposure itself. In our guinea-pig model, 6 -h daily conditioning exposure to an octave-band noise at 85 dB SPL reduces the permanent threshold shifts (PTSs) from a subsequent 4-h traumatic expo sure to the same noise band at 109 dB SPL, as assessed by both compound act ion potentials (CAPs) and distortion product otoacoustic emissions (DPOAEs) . The frequency region of maximum threshold protection is approximately one -half octave above the upper frequency cutoff of the exposure band. Protect ion is also evident in the magnitude of suprathreshold CAPs and DPOAEs, whe re effects are more robust and extend to higher frequencies than those evid ent at or near threshold. The conditioning exposure also enhanced cochlear sensitivity, when evaluated at the same postconditioning time at which the traumatic exposure would be delivered in a protection study. Response enhan cements were seen in both threshold and suprathreshold CAPs and DPOAEs. The frequency dependence of the enhancement effects differed, however, by thes e two metrics. For CAPs, effects were maximum in the same frequency reg lon as those most protected by the conditioning. For DPOAEs, enhancements were shifted to lower frequencies. The conditioning exposure also enhanced both ipsilaterally and contralaterally evoked olivocochlear (OC) reflex strengt h, as assessed using DPOAEs. The frequency and level dependence of the refl ex enhancements were consistent with changes seen in sound-evoked discharge rates in OC fibers after conditioning. However, comparison with the freque ncy range and magnitude of conditioning-related protection suggests that th e protection cannot be completely explained by amplification of the OC refl ex and the known protective effects of OC feedback. Rather, the present res ults suggest that sound conditioning leads to changes in the physiology of the outer hair cells themselves, che peripheral targets of the OC reflex.