Abstract
In humans, functional evidence based on recording cochlear microphonic, auditory nerve, and brain stem responses has shown that the site of lesion in hearing loss following neonatal hyperbilirubinemia is the auditory nerve (with sparing of the hair cells). Structural damage to the central nervous system (CNS) including the cochlear nuclei has been demonstrated in adult, homozygous Gunn rats which develop hyperbilirubinemia shortly after birth. In an attempt to use the Gunn rat as an experimental model for bilirubin-induced CNS damage, auditory nerve and brain stem responses (ABR) were recorded in jaundiced (homozygous) and non-jaundiced (heterozygous) Gunn rats and in Sabra (Wistar) rats. All of the rats including the jaundiced Gunn rats had normal ABR and responded behaviorally to sound stimuli. These results suggest that the adult jaundiced Gunn rat retains auditory function and in this way differs from human patients in whom neonatal jaundice has lead to hearing loss. Therefore, the adult homozygous Gunn rat probably cannot serve as a model for hearing loss due to hyperbilirubinemia.
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