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[12] and Frydman et al. [34] have demonstrated that mutation in a single human allele of Pou4f3 (Brn3c) results in a late onset of high frequency hearing loss. Thus far no data are available that correlate the late onset of hearing loss with morphological defects in the cochlea. In fact, an investigation of Brn3c heterozygotic mice showed no additional effect on hearing loss due to haploinsufficiency in these mice [35]. Our data on Brn3c null mouse mutants nevertheless suggest that the high to low frequency progressive hearing loss in humans may correlate with the unknown factor(s) that mediate apical spiral neuron survival into adulthood. Quantitative data on human Pou4f3 cochleae is needed to verify that spiral neuron loss is more pronounced in the basal, high frequency area of these hearing-deficient patients. Similar data are also needed for other congenitally deaf children [36] and in the deaf white cat [25]. Further work on the recently available mutant mice with specific absence of all hair cells [37], outer hair cells in the base [38] or apex [39] could further help to clarify the role of hair cells in forming and maintaining afferent and efferent innervation in these model mice."}

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