6533b82dfe1ef96bd12913a6
RESEARCH PRODUCT
COX-2 expression in the guinea pig cochlea is partly altered by moderate sound exposure.
Dirk SchäferUlf-riidiger HeinrichRalph FeltensAntje EimermacherJürgen BriegerOxana SelivanovaWolf J. Mannsubject
NeuronsGeneral NeuroscienceGuinea PigsGene ExpressionStimulationDose-Response Relationship RadiationSound perceptionAnatomyBiologyImmunohistochemistryCell biologyCochleaSound exposuremedicine.anatomical_structureAcoustic StimulationOrgan of CortiCyclooxygenase 2Spiral ligamentotorhinolaryngologic diseasesmedicineAnimalsInner earsense organsSpiral ganglionCochleadescription
The cyclooxygenase-2 isoform (COX-2) was found recently to be constitutively expressed in the guinea pig inner ear. To gain knowledge about its role in sound perception, alterations in the COX-2 level of moderate noise-stimulated cochleae were determined. Staining intensities were quantified in different regions using an immunohistochemical staining procedure and computer-assisted system. After 70 dB and 90 dB noise exposure for 1 h at 8000 Hz, COX-2 downregulation was observed in the organ of Corti, which was most prominent in Deiters' cells near Hensen cells and outer hair cells. In pillar cells, COX-2 levels were only slightly reduced after 70 dB but strongly diminished after 90 dB exposure. In Hensen cells, COX-2 was downregulated after 70 dB stimulation, revealing a decreasing COX-2 content from the third to the first turn of the cochlea and a homogeneously reduced enzyme expression in all three turns after 90 dB. The COX-2 content in inner hair cells was nearly identical to unexposed cochleae after 70 dB exposure but significantly reduced after 90 dB stimulation. In spiral ganglion cells, stria vascularis, spiral ligament and limbus, COX-2 expression was unchanged after 70 dB and 90 dB. We suggest that alterations in COX-2 expression might contribute to diminished sensitivity at the cochlea after noise exposure to reduce subsequent noise distress, termed sound conditioning.
year | journal | country | edition | language |
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2006-02-01 | Neuroscience letters |