title: Temporary reduction of distortion product otoacoustic emissions (DPOAEs) immediately following auditory brainstem response (ABR).
abstract: The hearing status of an experimental animal is typically assessed in the laboratory setting by the combined use of auditory brainstem response (ABR) and distortion product otoacoustic emissions (DPOAEs), carried out in succession, with the former assay preceding the latter. This study reports a cautionary finding that the use of this accepted regimen yields a reduced DPOAE response. When the DPOAEs were performed after ABR testing, transient reduction of the DPOAE amplitudes was observed at all frequencies in both the inbred, C57/B6 and FVB/N, and the outbred, SW mouse strains. DPOAEs were reduced post-ABR in multiple mouse strains which suggests that this finding is not strain-specific but a general consequence of the preceding ABR analysis. The reduction in DPOAE was temporary: when re-tested at one hour, DPOAE amplitudes recovered to pre-ABR levels. In contrast to the ABR's impact on DPOAE response, ABR thresholds were not altered or reduced when preceded immediately by DPOAE measurements. The molecular alterations underlying the ABR-induced transient reduction of DPOAE remain to be determined. To investigate the potential role of reactive oxygen species in post-ABR DPOAE reduction, transgenic mice over-expressing SOD1, the cytoplasmic enzyme critical for removal of superoxide radicals were subjected to the same auditory testing regimen. Similar to their wild type littermates, the SOD1 transgenic mice also demonstrated post-ABR DPOAE reduction, and thus do not support a role for superoxide radicals in transient reduction of DPOAE. While toxic noise exposure is known to negatively impact OAE, transient decrease in DPOAE levels following standard ABR assay has not been previously described. A practical outcome from this study is a recommendation for reversal of the traditional order for carrying out auditory tests, with the OAE measurements preceding ABR assessment, thus ensuring that the DPOAE response is unaffected.
authors.affiliation: Department of Otolaryngology, New York University School of Medicine, New York, NY 10016, USA. anand.mhatre@nyumc.org
authors.forename: Anand N
authors.initials: AN
authors.lastname: Mhatre
authors.forename: Bobby
authors.initials: B
authors.lastname: Tajudeen
authors.forename: Elena M
authors.initials: EM
authors.lastname: Welt
authors.forename: Christopher
authors.initials: C
authors.lastname: Wartmann
authors.forename: Glenis R
authors.initials: GR
authors.lastname: Long
authors.forename: Anil K
authors.initials: AK
authors.lastname: Lalwani
mesh_terms: D000818:Animals; D001309:Auditory Threshold; D016057:Evoked Potentials, Auditory, Brain Stem / Q000502:physiology*; D006198:Hair Cells, Auditory / Q000502:physiology*; D006320:Hearing Tests; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D023421:Models, Animal; D017084:Otoacoustic Emissions, Spontaneous / Q000502:physiology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism; D000072105:Superoxide Dismutase-1
chemical_list: D017382:Reactive Oxygen Species; C000606291:Sod1 protein, mouse; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1