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 su ggested 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, Aud itory brainstem evoked response and distortion product otoacoustic emission s appear similar as in the control group. A moderate noise-induced trauma p roduced 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 do es not provide physiological protection against a moderate noise-induced in ner ear trauma in mice. Copyright (C) 2000 S. Karger AG, Basel.