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WDR1 expression in normal and noise‐damaged Sprague‐Dawley rat cochleae
Author(s) -
Song JaeJin,
Adler Henry J.,
Lee Ho Sun,
Jang Jeong Hun,
Park MinHyun,
Lee Jun Ho,
Chang Sun O,
Oh Seung Ha
Publication year - 2013
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.23197
Subject(s) - biology , neuroscience , noise (video) , expression (computer science) , medicine , artificial intelligence , computer science , image (mathematics) , programming language
WD40 repeat protein 1 (WDR1) has been suggested as a protective mechanism or a sign of regeneration in avian cochlea. However, its role in mammalian cochlea has yet to be determined. Hence, we investigated WDR1 expression in sound‐overstimulated Sprague‐Dawley rats. Rats were divided into three groups (the permanent and temporary threshold shift [PTS and TTS] groups and the control group) according to the extent of noise exposure and euthanized immediately, 3, or 7 days after noise exposure for cochlear harvest. Immunocytochemistry localized WDR1 to outer hair cells, Deiter's cells, outer sulcus cells, and Reissner's membrane in the control group, and the PTS and TTS groups exhibited stronger WDR1 expression in the same cochlear regions than the controls. Moreover, WDR1 expression in these noise‐exposed groups was extended to inner hair cells and basal cells of the stria vascularis. The expression of WDR1 in the PTS and TTS groups showed differences in intensity and shifts of localization, based on exposure length and recovery duration. Contrary to the avian cochlea, hair cell regeneration does not naturally occur in the acoustically damaged mammalian cochlea. Therefore, elevated WDR1 expression after acoustic overstimulation in the current experiments may provide a mechanism for protection against noise exposure. J. Comp. Neurol. 521:1470–1481, 2013. © 2012 Wiley Periodicals, Inc.