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Resistance to neomycin ototoxicity in the extreme basal (hook) region of the mouse cochlea.

Authors :
Lin SCY
Thorne PR
Housley GD
Vlajkovic SM
Source :
Histochemistry and cell biology [Histochem Cell Biol] 2018 Sep; Vol. 150 (3), pp. 281-289. Date of Electronic Publication: 2018 Jun 04.
Publication Year :
2018

Abstract

Aminoglycoside ototoxicity results in permanent loss of the sensory hair cells in the mammalian cochlea. It usually begins at the basal turn causing high-frequency hearing loss. Here we describe previously unreported resistance of hair cells to neomycin ototoxicity in the extreme basal (hook) region of the developing cochlea of the C57BL/6 mouse. Organ of Corti explants from mice at postnatal day 3 were incubated (37 °C, 5% CO <subscript>2</subscript> ) in normal culture medium for 19.5 h prior to and after exposure to neomycin (1 mM, 3 h). To study neomycin uptake in the hair cells, cochlear explants were incubated with Neomycin Texas-red (NTR) conjugate. As expected, exposure to neomycin significantly reduced the survival of inner (IHC) and outer hair cells (OHC). IHC survival rate was high in the apical segment and low in the basal segment. OHC were well preserved in the apical and hook regions, with substantial OHC loss in the basal segment. The NTR uptake study demonstrated that the high survival rate in the extreme basal turn OHC was associated with low NTR uptake. Treatment with a calcium chelator (BAPTA), which disrupts the opening of mechanoelectrical (MET) transduction channels, abolished or reduced NTR uptake in the hair cells throughout the cochlea. This confirmed the essential role of MET channels in neomycin uptake and implied that the transduction channels could be impaired in the hook region of the developing mouse cochlea, possibly as a result of the cadherin 23 mutation responsible for the progressive deafness in C57BL/6 mice.

Details

Language :
English
ISSN :
1432-119X
Volume :
150
Issue :
3
Database :
MEDLINE
Journal :
Histochemistry and cell biology
Publication Type :
Academic Journal
Accession number :
29862415
Full Text :
https://doi.org/10.1007/s00418-018-1683-8