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ABSTRACT: The aims of this study were to explore the correlation between DPOAE adaptation magnitude in three different guinea pig strains to examine if the genetic component affects the DPOAE adaptation magnitude. It was also to investigate the correlation between strains with certain characteristics i.e. reduced susceptibility to noise, and early onset of age-dependent hearing loss and the DPOAE adaptation magnitude. The animals were anaesthetized and the 2f1-f2 DPOAE (f1=8k Hz, and f2/f1=1.2) adaptation was established with a minimum of 144 combinations of f1; f2 where f1 was held fixed and f2 was varied in 1 dB or 0.4 dB steps. The DPOAE adaptation magnitude was defined as the difference between maximum positive level and the maximum negative level. ABRs were conducted at different age-groups (at 4, 6.3, and 12.5k Hz) to evaluate the progress of hearing thresholds by age. There was a significant difference between strains regarding the hearing loss at one year of age. There was no significant difference in DPOAE adaptation magnitude between strains included in this study and from this we conclude that the DPOAE adaptation magnitude is not a predictor for the susceptibility to noise trauma, or early onset of age-dependent hearing loss, using the methods described in this paper.
Hearing Research 03/2007; 224(1-2):27-33. · 2.70 Impact Factor
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ABSTRACT: We applied the dopaminergic (DA) neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the guinea pig cochlear perilymph. Immunolabeling of lateral olivocochlear (LOC) neurons using antibodies against synaptophysin was reduced after the MPTP treatment. In contrast, labeling of the medial olivocochlear innervation remained intact. As after brainstem lesions of the lateral superior olive (LSO), the site of origin of the LOC neurons, the main effect of disrupting LOC innervation of the cochlea via MPTP was a depression of the amplitude of the compound action potential (CAP). CAP amplitude depression was similar to that produced by LSO lesions. Latency of the N1 component of the CAP, and distortion product otoacoustic emission amplitude and adaptation were unchanged by the MPTP treatment. This technique for selectively lesioning descending LOC efferents provides a new opportunity for examining LOC modulation of afferent activity and behavioral measures of perception.
Journal of the Association for Research in Otolaryngology 04/2005; 6(1):48-62. · 2.84 Impact Factor
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Tamar Ben-Yosef,
Inna A Belyantseva,
Thomas L Saunders,
Elizabeth D Hughes,
Kohei Kawamoto,
Christina M Van Itallie,
Lisa A Beyer, Kärin Halsey,
Donald J Gardner,
Edward R Wilcox,
Julia Rasmussen,
James M Anderson,
David F Dolan,
Andrew Forge,
Yehoash Raphael,
Sally A Camper,
Thomas B Friedman
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ABSTRACT: Tight junctions (TJs) create ion-selective paracellular permeability barriers between extracellular compartments. In the organ of Corti of the inner ear, TJs of the reticular lamina separate K(+)-rich endolymph and Na(+)-rich perilymph. In humans, mutations of the gene encoding claudin 14 TJ protein cause profound deafness but the underlying pathogenesis is unknown. To explore the role of claudin 14 in the inner ear and in other tissues we created a mouse model by a targeted deletion of Cldn14. In the targeted allele a lacZ cassette is expressed under the Cldn14 promoter. In Cldn14-lacZ heterozygous mice beta-galactosidase activity was detected in cochlear inner and outer hair cells and supporting cells, in the collecting ducts of the kidney, and around the lobules of the liver. Cldn14-null mice have a normal endocochlear potential but are deaf due to rapid degeneration of cochlear outer hair cells, followed by slower degeneration of the inner hair cells, during the first 3 weeks of life. Monolayers of MDCK cells expressing claudin 14 show a 6-fold increase in the transepithelial electrical resistance by decreasing paracellular permeability for cations. In wild type mice, claudin 14 was immunolocalized at hair cell and supporting cell TJs. Our data suggest that the TJ complex at the apex of the reticular lamina requires claudin 14 as a cation-restrictive barrier to maintain the proper ionic composition of the fluid surrounding the basolateral surface of outer hair cells.
Human Molecular Genetics 09/2003; 12(16):2049-61. · 7.64 Impact Factor
