Pillar cells with their rich network of tubulin and actin filaments have been reported to contribute to the rigidity of the organ of Corti. As the earliest expression of the actin filament enhancer vasodilator-stimulated phosphoprotein (VASP) in the outer pillar head plate has been found to be associated with the onset of hearing, we tested hearing development in VASP–/– compared to wild-type mice. Performing measurements of auditory brainstem responses on postnatal days (P) P14 and P21, we detected statistically significantly higher thresholds in VASP–/– compared to wild-type mice at P14, but no hearing differences at P21. Staining for prestin and synaptophysin at P12 in morphologically regularly developed cochleae of VASP–/– mice provided an immature prestin protein pattern but no evidence of developmental delay in hair cell innervations. Regularly intense staining of actin filaments in the outer pillar head plate was found only in wild-type but not in VASP–/– mice at P14. At P21, intensive actin filament staining was also observed in the outer pillar head plates of VASP–/– mice. The delayed hearing development in VASP–/– mice is supposed to be caused by a delayed formation of actin filaments in the outer pillar head plate indicating the importance of appropriate pillar cell stiffness in cochlear mechanics.

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