Lack of calbindin-D28k does not affect hearing level or survival of hair cells in acoustic trauma.

Calbindin is a cytosolic calcium-binding protein abundant in the hair cells of the inner ear and in distinct neurons of the auditory pathway. It is suggested to speed the return of potentially toxic calcium levels to normal. In this study, we show the basic hearing functions and the result of noise trauma from the calbindin null mutant mice generated by gene targeting. Auditory brainstem evoked response and distortion product otoacoustic emissions appear similar as in the control group. A moderate noise-induced trauma produced a similar loss of hair cells in calbindin null mutant mice than in wild-type controls. The result suggests that although calbindin is abundant in hair cells, it is not essential for the main hearing function and it does not provide physiological protection against a moderate noise-induced inner ear trauma in mice.