Auditory nerve of the normal and jaundiced rat. I. Spontaneous discharge rate and cochlear nerve histology

Abstract

Hyperbilirubinemia is a major problem in neonatal intensive care. Hearing impairment is one of its sequelae. Although lesions of the central auditory pathways are known to be associated with this disorder in both humans and homozygous Gunn rats, the presence of cochlear pathology is still controversial. The purpose of this study was to examine the functional integrity of the peripheral auditory system in the Gunn rat. The Gunn rat is a mutant of the Wistar strain with congenital deficiency of the liver enzyme uridine diphosphoglucuronyl transferase which is essential for bilirubin conjugation. This deficiency is inherited as an autosomal recessive trait, with the homozygous animals (jj) showing evidence of bilirubin encephalopathy. The heterozygotes (Jj) have 50% enzyme deficiency and are not jaundiced. The Long-Evans rat served as a control. The approach was to study the discharge characteristics of single auditory nerve fibers using standard procedures in a closed and calibrated sound system. Various response measurements which would reveal pathological processes in the cochlea were analyzed. In this study, spontaneous discharge rate distribution and interspike interval statistics derived from Gunn rat auditory nerve recording were found to be within the normal range, and cochlear nerve histology showed no evidence of neuropathy.