2021
Efferent neurons control hearing sensitivity and protect hearing from noise through the regulation of gap junctions between cochlear supporting cells
Zhao H, Liu L, Yu N, Zhu Y, Mei L, Chen J, Liang C. Efferent neurons control hearing sensitivity and protect hearing from noise through the regulation of gap junctions between cochlear supporting cells. Journal Of Neurophysiology 2021, 127: 313-327. PMID: 34907797, PMCID: PMC8759971, DOI: 10.1152/jn.00468.2021.Peer-Reviewed Original ResearchConceptsOuter hair cellsActive cochlear amplificationCochlear efferent systemDistortion product otoacoustic emissionsEfferent systemEfferent pathwaysHearing sensitivityMedial olivocochlear efferent fibersPresynaptic vesicular acetylcholine transportersGap junctionsOlivocochlear efferent fibersHair cellsApplication of acetylcholineCochlear supporting cellsProtection of hearingVesicular acetylcholine transporterActive cochlear amplifierCochlear amplificationPostsynaptic ACh receptorsProduct otoacoustic emissionsMOC efferent systemHair cell activityEfferent nervesEfferent inhibitionEfferent fibers
2019
Hearing loss is an early biomarker in APP/PS1 Alzheimer’s disease mice
Liu Y, Fang S, Liu L, Zhu Y, Li C, Chen K, Zhao H. Hearing loss is an early biomarker in APP/PS1 Alzheimer’s disease mice. Neuroscience Letters 2019, 717: 134705. PMID: 31870800, PMCID: PMC7004828, DOI: 10.1016/j.neulet.2019.134705.Peer-Reviewed Original ResearchConceptsAPP/PS1 AD miceDistortion product otoacoustic emissionsAuditory brainstem responseAD miceHearing lossAlzheimer's diseaseDisease miceAPP/PS1 Alzheimer's disease miceAPP/PS1 miceAD mouse modelAlzheimer's disease miceMedial geniculate bodyWild-type littermatesCochlear microphonic recordingsProduct otoacoustic emissionsMonths of ageSpatial learning deficitsPS1 miceUpper brainstemABR thresholdFunction testingGeniculate bodyBrainstem responseLateral lemniscusEarly biomarkers
2018
Knockout of Pannexin-1 Induces Hearing Loss
Chen J, Liang C, Zong L, Zhu Y, Zhao H. Knockout of Pannexin-1 Induces Hearing Loss. International Journal Of Molecular Sciences 2018, 19: 1332. PMID: 29710868, PMCID: PMC5983795, DOI: 10.3390/ijms19051332.Peer-Reviewed Original ResearchConceptsDistortion product otoacoustic emissionsHearing lossKO miceKO mouse lineMouse linesCochlear microphonicsAuditory brainstem response thresholdActive cochlear amplificationPanx1 KO miceAuditory function testsProduct otoacoustic emissionsKnockout mouse lineFunction testsNonsyndromic hearing lossABR thresholdHearing functionHigh incidenceRecent studiesGap junctional proteinReceptor currentsOtoacoustic emissionsMiceCochlear amplificationConsistent phenotypeResponse threshold
2015
Pannexin 1 deficiency can induce hearing loss
Zhao H, Zhu Y, Liang C, Chen J. Pannexin 1 deficiency can induce hearing loss. Biochemical And Biophysical Research Communications 2015, 463: 143-147. PMID: 26002464, PMCID: PMC4464954, DOI: 10.1016/j.bbrc.2015.05.049.Peer-Reviewed Original ResearchConceptsDistortion product otoacoustic emissionsHearing lossAuditory brainstem response recordingsProgressive hearing lossProduct otoacoustic emissionsHigh incidenceCell degenerationOtoacoustic emissionsGap junction proteinAcoustic stimulationCell apoptotic pathwaysHair cellsResponse recordingsGene mutationsJunction proteinsExtensive expressionCochleaActive cochlear mechanicsGap junctionsApoptotic pathwayDeficiencyHearingCritical roleCochlear mechanics
2014
Connexin26 (GJB2) deficiency reduces active cochlear amplification leading to late-onset hearing loss
Zhu Y, Chen J, Liang C, Zong L, Chen J, Jones R, Zhao H. Connexin26 (GJB2) deficiency reduces active cochlear amplification leading to late-onset hearing loss. Neuroscience 2014, 284: 719-729. PMID: 25451287, PMCID: PMC4268423, DOI: 10.1016/j.neuroscience.2014.10.061.Peer-Reviewed Original ResearchConceptsLate-onset hearing lossActive cochlear amplificationDistortion product otoacoustic emissionsHearing lossNonsyndromic hearing lossTherapeutic interventionsProgressive hearing lossHair cell lossPostnatal day 5Cochlear amplificationProduct otoacoustic emissionsConditional knockout miceKnockout miceClinical observationsDay 5Cell lossEndocochlear potentialOtoacoustic emissionsNormal hearingCx26 expressionDeafness mechanismMiceCx26 deficiencyCochleaIntervention
2013
Active cochlear amplification is dependent on supporting cell gap junctions
Zhu Y, Liang C, Chen J, Zong L, Chen G, Zhao H. Active cochlear amplification is dependent on supporting cell gap junctions. Nature Communications 2013, 4: 1786. PMID: 23653198, PMCID: PMC3675877, DOI: 10.1038/ncomms2806.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAuditory ThresholdCochlear Microphonic PotentialsConnexin 26ConnexinsEvoked Potentials, Auditory, Brain StemGap JunctionsGene DeletionGene TargetingHair Cells, Auditory, OuterHearing LossLabyrinth Supporting CellsMiceMice, KnockoutMolecular Motor ProteinsNonlinear DynamicsOtoacoustic Emissions, SpontaneousSpiral GanglionConceptsActive cochlear amplificationOuter hair cellsCell gap junctionsHearing lossCochlear amplificationHair cellsGap junctionsDistortion product otoacoustic emissionsOuter hair cell electromotilityHair cell electromotilitySevere hearing lossProduct otoacoustic emissionsShorter outer hair cellsHair-bundle movementsOuter pillar cellsLeftward shiftOtoacoustic emissionsAcoustic stimulationDeiters' cellsHearing sensitivityConnexin 26Active cochlear mechanicsNovel findingsPillar cellsBundle movement
2008
Prestin up-regulation in chronic salicylate (aspirin) administration: An implication of functional dependence of prestin expression
Yu N, Zhu M, Johnson B, Liu Y, Jones R, Zhao H. Prestin up-regulation in chronic salicylate (aspirin) administration: An implication of functional dependence of prestin expression. Cellular And Molecular Life Sciences 2008, 65: 2407-2418. PMID: 18560754, PMCID: PMC2548279, DOI: 10.1007/s00018-008-8195-y.Peer-Reviewed Original ResearchConceptsLong-term administrationPrestin expressionSalicylate administrationChronic salicylate administrationDistortion product otoacoustic emissionsNuclear transcription factors c-fosProduct otoacoustic emissionsTranscription factor c-FosOHC electromotilityHearing lossNF-κBAcute inhibitionOtoacoustic emissionsAdministrationC-fosProtein levelsOuter hair cell electromotilityHair cell electromotilityEgr-1Incremental increaseExpressionSalicylateElectromotilityFour-fold
2004
Paradoxical Enhancement of Active Cochlear Mechanics in Long-Term Administration of Salicylate
Huang Z, Luo Y, Wu Z, Tao Z, Jones R, Zhao H. Paradoxical Enhancement of Active Cochlear Mechanics in Long-Term Administration of Salicylate. Journal Of Neurophysiology 2004, 93: 2053-2061. PMID: 15590729, DOI: 10.1152/jn.00959.2004.Peer-Reviewed Original ResearchConceptsDistortion product otoacoustic emissionsLong-term administrationOtotoxic mechanismsLong-term salicylate administrationAwake guinea pigsReversible hearing lossSalicylate-induced tinnitusActive cochlear mechanicsProduct otoacoustic emissionsInitial normal levelsDistortion productsSalicylate administrationSodium salicylateDaily injectionsSaline injectionHearing functionHearing lossCubic distortion productSingle injectionControl animalsOHC levelsCommon drugsSalicylate treatmentAcoustic emissionRate of recovery