Restraint stress and protection from acoustic injury in mice

The phenomenon of 'conditioning', whereby prior exposure to moderate-level non-traumatic sound reduces the permanent injury to subsequent high-level sound exposures, is suggestive of protective effects mediated by stress-induced gene expression in other systems. To test the role of stress pathways in acoustic injury, this study investigated the effect of mild physical restraint, a classic non-acoustic elicitor of stress, on vulnerability to subsequent noise-induced hearing loss. CBA/CaJ mice were divided into groups (control, restraint-only, restraint pre-trauma, and trauma-only), and cochlear sensitivity was assessed via compound action potentials and distortion product otoacoustic emissions. Results showed that two 12-h epochs of mild physical restraint significantly reduced permanent threshold shifts from a subsequent acoustic overexposure, as long as the treatment-trauma interval was short (2 h). Concurrent measures of circulating glucocorticoids showed that the period of protection coincided with the period of elevated corticosterone. Results are consistent with the idea that cochlear protective effects may be mediated by stress pathways and that glucocorticoid levels may be an important upstream regulator of these effects.