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Expression of Calcium Binding Proteins in the Auditory Brainstem Pathway of the Jaundiced Gunn Rat † 829

Sensorineural hearing loss is one of the major sequelae of neonatal hyperbilirubinemia. Retrocochlear sites of lesions due to kernicterus are related to significant abnormalities in the wave latencies, interwave intervals, and amplitudes of the auditory brainstem response. In the present study, changes in the expression of the calcium binding proteins (CBP) parvalbumin and calbindin-D28k have been examined in the homozygous recessive jaundiced (jj) Gunn rat by light microscopic immunohistochemistry at 15-18 days postnatally. The density of immunoreactive staining for both CBPs was reduced in the cochlear nuclei and the superior olivary complex, particularly the superior paraolivary and medial superior olivary nuclei, in comparison to age-matched heterozygous (Nj) control rats. At both sites, the extent of the reduction in immunoreactivity was related to the severity of the clinical symptoms. By contrast, immunoreactive staining in other brainstem auditory(e.g., dorsal and ventral nuclei of the lateral lemniscus, inferior colliculus, medial geniculate body) and neighboring non-auditory structures was similar in jaundiced and control rats. The developmental retardation of CBPs coincides with the period of synaptic refinement in the auditory brainstem, and the inability to buffer intracellular calcium effectively may lead to bilirubin-induced neuronal cell death, possibly by inhibition of Ca2+/calmodulin-dependent kinase II activity.