Narrow Results

Understanding the nonlinear capacitance (NLC) of prestin and outer hair cell (OHC) is important for exploring the activity of mammalian cochlea. After introducing a nontransporting five-state model of the OHC motor which is the tetramer of prestin, we obtain the peak of the NLC of OHC and the peak shift of the NLC as functions of the concentration of the intracellular Cl^- anions. By employing the same model, we calculate the frequency dependence of the NLC as well. The model results both in equilibrium state and of the frequency dependence agree with the experimental observations. Accordingly, it suggests that the introduced five-state model is a candidate for exploring the NLC of both OHC and prestin.

Intense sound exposure causes permanent hearing loss due to hair cell and cochlear damage. Prior conditioning with sublethal stressors, such as non-traumatic sound, heat stress and restraint protects ear from acoustic injury. To explore the mechanisms of conditioning-induced cochlear protection, Young's modulus and the amount of filamentous actin (F-actin) of mouse outer hair cells (OHCs) with heat stress and those without such stress were investigated by atomic force microscopy (AFM) and confocal laser scanning microscopy (CLSM), respectively. Heat stress caused an increase in Young's modulus of OHCs at 3–6 h after its application along with an increase in their amount of F-actin. These time courses are similar to the previous report in which heat stress was shown to suppress permanent threshold shift. These results indicate that heat stress structurally modifies OHCs to increase their F-actin and thereby renders them stiffer, resulting in protection of ear from acoustic injury.