2017
Hypothesis of K+-Recycling Defect Is Not a Primary Deafness Mechanism for Cx26 (GJB2) Deficiency
Zhao H. Hypothesis of K+-Recycling Defect Is Not a Primary Deafness Mechanism for Cx26 (GJB2) Deficiency. Frontiers In Molecular Neuroscience 2017, 10: 162. PMID: 28603488, PMCID: PMC5445178, DOI: 10.3389/fnmol.2017.00162.Peer-Reviewed Original ResearchHearing lossDeafness mechanismCx26 deficiencyInner ear gap junctionsHair cell degenerationNonsyndromic hearing lossDisruption of permeabilityCongenital deafnessCell degenerationHair cellsHair cell excitationHereditary deafnessCell excitationConnexin26 MutationsGap junctional channelsGap junctionsDevelopmental disordersDeficiencyDeafnessExtracellular spaceReview articleJunctional channelsDegeneration
2005
Gap junctional hemichannel-mediated ATP release and hearing controls in the inner ear
Zhao H, Yu N, Fleming C. Gap junctional hemichannel-mediated ATP release and hearing controls in the inner ear. Proceedings Of The National Academy Of Sciences Of The United States Of America 2005, 102: 18724-18729. PMID: 16344488, PMCID: PMC1317927, DOI: 10.1073/pnas.0506481102.Peer-Reviewed Original ResearchConceptsHemichannel-mediated ATP releaseHair cellsGap junctional blockerActive cochlear amplifierAuditory sensory hair cellsSensory hair cellsEffect of ATPP2 receptorsExtracellular Ca2OHC electromotilityCochlear sensitivityATP releaseConnexin gap junctionsExtracellular ATPConnexin expressionInner earImmunofluorescent stainingHearing controlsHearing sensitivityOuter hair cell electromotilityCochleaHair cell electromotilityConnexin hemichannelsCochlear fluidsGap junctional channels