Immunohistochemical Expressions of TrkB and TrkC Receptors in Rat Cochleas with Amikacin-induced Ototoxicity

Park, So Young; Chae, Sa Yong

Abstract

BACKGROUND AND OBJECTIVES: Neurotrophins have been known to be responsible for the differentiation and survival of developing neurons as well as for aiding the recovery of adult neurons from injury. The neurotrophin family includes NGF, BDNF, NT-3, and NT-4/5, and they exert their biological functions through activation of the high-affinity binding receptors, that is trkA, trkB, and trkC, with high characteristic specificity. Previous studies indicate that spiral ganglion cells express trkB and trkC mRNAs, while auditory hair cells produce NT-3 mRNA that directly affect maturation and survival of auditory neurons. It has been reported that the loss of target innervation and the eventual degeneration of auditory neurons caused by aminoglycoside ototoxicity can be prevented by the infusion of neurotrophic factors. The purpose of this study is to provide the expression patterns of trkB and trkC in the normal chochleas and damaged cochleas with aminoglycoside ototoxicity.
MATERIALS AND METHODS
Adult Sprague-Dawley rats were treated with amikacin 500 mg/kg for ten days, and sacrificed on the 7th, 14th, 21th, and 28th day following the last injection. Auditory brainstem response was measured in each animal. Immunohistochemical method was used to study the localization of trkB and trkC receptors in the cochleas of adult rats of either normal control group or ototoxicity group.
RESULTS
Immunoreactivities to trkB and trkC receptors were strongly positive in the spiral ganglion cells of all cochleas, especially in the neuronal perikarya of the type I cells. No difference in staining pattern was seen among the cochleas with different hearing thresholds.
CONCLUSION
The uniform expression pattern of trkB and trkC receptors in the spiral ganglion cells regardless of the degree of ototoxicity suggests that neurotrophic factors may bind to these receptors to initiate the cellular mechanisms for neuronal survival in the injured auditory system.