简介：Hearinglossisoneofthemostfrequenthealthissuesinindustrializedcountries.Thepathogenesisandmolecularmechanismsofhearinglossarestillunclear.Histonedeacetylases(HDACs)areemergingaskeyenzymesinmanyphysiologicalprocesses,includingchromatinremodeling,regulationoftranscription,DNArepair,metabolism,genomestabilityandproteinsecretion.RecentstudiesindicatedthatHDACsareassociatedwiththedevelopmentandprogressionofhearingloss.DysfunctionofHDACscouldpromotetheoxidativestressandagingintheinnerear.Inlightofconsideringthecurrentstagnationinthedevelopmentoftherapeuticoptions,theneedfornewstrategiesinthetreatmentofhearinglosshasneverbeensopressing.Inthisreview,wewillsummarizethereportedliteraturesforHDACsinhearinglossanddiscusshowHDACfamilymembersshowdifferentperformancesforthepossibilityofprocessofdiseasesdevelopment.Thepossibilityofpharmacologicalinterventiononhearinglossopensanovelpathinthetreatmentofhearingloss.

简介：Inthisstudy,Ifocusedonfindingameanofprotectingagainsthearingloss.Byinfusingthecochleawiththeneurotrophinfactor,NT-3aloneorcombinedtreatmentwithMK801,aNMDAreceptorantagonistIfoundhearinglosswasattenuatedandspiralganglionneuronlosswasnearlytotallyprotectedindicatingthattheimportanceofthecombinedtreatmentofNT-3andNMDAreceptorantagonistsinthetreatmentofhearingdisorders.

简介：ObjectiveChronictinnitusisahighlyprevalentconditionandhasbeenhypothesizedtoresultfromaninnatedisturbanceincentralnervousserotonergictransmission.Giventhefrequentcomorbiditywithmajordepressionandanxiety,wearguethatcandidategenesforthesedisordersarelikelytooverlap.Thepresentstudyaddressesthegeneencodingforthe5-HT1Areceptorasaputativeriskfactorfortinnitus.MethodsIn88subjectswithadiagnosisofchronicsubjectivetinnituswhounderwentadetailedneurootologicalexamination,theentire5-HT1AgenewasamplifiedusingoverlappingPCRproducts.Ampliconswerecustomsequencedbidirectionallyandwerescreenedforvariantsinmultiplealignmentsagainstthehumangenomereference.ResultsWeidentifiedasynonymousC>Texchangeatresidue184(Pro)in7/88subjects,butdetectednomissensevariantsinthepopulationunderstudy.Specifically,thefollowingresidueswerefullyconserved:16(Pro),22(Gly),28(Ile),98(Val),220(Arg),267(Val),273(Gly),and418(Asn).DiscussionThepresentdatacountagainstthecausationofchronictinnitusbyachangeinthe5-HT1Areceptor'saminoacidsequence.However,theallelefrequencyforthe184Prominorallele(0.04)reachedtwicethefrequencyreportedincontrolcohortsfromthesameethnicity.Additionalinvestigationsareinvitedtoclarifytheroleofthe5-HT1Apolymorphisminlargersamples,andtocontrolforcomorbidaffectivedisorders.

简介：Durationisasalientfeatureofacousticsignalsincludingspeech.Durationtuningwasfirstreportedinfrogsandlaterinecholocatingbats.Morerecently,durationtuninghasbeenreportedinnon-echolocatingmammalsandappearstobeafundamentalencodingmechanismthroughouttheanimalkingdom.However,thedurationtuningreportedinthesenon-echolocatingmammalsappearstobemuchweakerthanthatinthepreviousstudiesonbats.Incontrasttothisfinding,ourrecentstudyreportedthatdurationtuningintheICinguineapigsappearedtobestrongwhenitwasmeasuredusinganappropriatetemporalwindow.Withsuchatemporalwindow,durationtuningwasfoundtobecompatiblewiththatofecho-locatingbats.Inthepresentreport,wefurtherdemonstratethatdurationtuningintheICofthisspeciesisestablishedbyinteractionbetweenexcitationandGABAergicinhibition.Inadditiontooverallincreaseinresponsiveness,applicationofbicuculline(BIC),aGABA-Areceptorantagonist,wasfoundtosignificantlyreduceoreliminatedurationselectivityin44outofthe67neuronsthatshowedcleardurationtuningfromasampleof340neurons.

简介：Thedevelopmentandplasticityofcentralauditorysystemcanbeinfluencedbythechangeofperipheralneuronalactivity.However,themolecularmechanismparticipatingintheprocessremainselusive.Brain-derivedneurotrophicfactor(BDNF)bindingwithitsfunctionalreceptortropomyosinreceptorkinaseB(TrkB)hasmultipleeffectsonneurons.Hereweusedaratmodelofauditorydeprivationbybilateralcochlearablation,toinvestigatethechangesinexpressionofBDNFandTrkBintheauditorycortexafterauditorydeprivationthatoccurredduringthecriticalperiodforthedevelopmentofcentralauditorysystem.Reversetranscription-quantitativepolymerasechainreaction(RTqPCR)andimmunohistochemistrymethodswereadoptedtodetectthemRNAandproteinexpressionlevelsofBDNFandTrkBintheauditorycortexat2,4,6and8weeksaftersurgery,respectively.ThechangeintheexpressionofBDNFandTrkBmRNAsandproteinsfollowedsimilartrend.Inthebilateralcochlearablationgroups,theBDNF-TrkBexpressionlevelinitiallydecreasedat2weeksbutincreasedat4weeksfollowedbythereductionat6and8weeksaftercochlearremoval,ascomparedtotheage-matchedshamcontrolgroups.Inconclusion,theBDNF-TrkBsignalingisinvolvedintheplasticityofauditorycortexinanactivity-dependentmanner.