简介：Trimethyltin(TMT)isanoccupationalandenvironmentalhealthhazardbehavingasapotentneurotoxinknowntoaffectthecentralnervoussystemaswellastheperipheralauditorysystem.However,themechanismsunderlyingTMT-inducedototoxicityarepoorlyunderstood.ToelucidatetheeffectsofTMTonthecochlea,asingleinjectionof4or8mg/kgTMTwasadministeredintraperitoneallytoadultrats.Thecompoundactionpotential(CAP)thresholdwasusedtoassessthefunctionalstatusofthecochleaandhistologicaltechniqueswereusedtoassesstheconditionofthehaircellsandauditorynervefibers.TMTat4mg/kgproducedatemporaryCAPthresholdelevationof25-60dBthatrecoveredby28dpost-treatment.Althoughtherewasnohaircelllosswiththe4mg/kgdose,therewasanoticeablelossofauditorynervefibersparticularlybeneaththeinnerhaircells.TMTat8mg/kgproducedalargepermanentCAPthresholdshiftthatwasgreatestatthehighfrequencies.TheCAPthresholdshiftwasassociatedwiththelossofouterhaircellsandinnerhaircellsinthebasal,high-frequencyregionofthecochlea,considerablelossofauditorynervefibersandasignificantlossofspiralganglionneuronsinthebasalturn.Spiralganglionneuronsshowedevidenceofsomashrinkageandnuclearcondensationandfragmentation,morphologicalfeaturesofapoptoticcelldeath.TMT-induceddamagewasgreatestinthehigh-frequency,basalregionofthecochleaandthenervefibersbeneaththeinnerhaircellswerethemostvulnerablestructures.

简介：Introduction:Theabsenceofvertigoduringthecalorictest,despitearobustresponse,hasbeensuggestedtorepresentacentralvestibularsystemphenomenon.Thepurposeofthisinvestigationwastodeterminetheprevalenceofabsentcaloric-inducedvertigoperceptioninanunselectedgroupofpatientsandtoassesspossiblepredictingvariables.Methods:Prospectiveinvestigationof92unselectedpatientswhounderwentcalorictesting.Inclusioncriteriawerethateachpatientgenerateamaximumslowphasevelocity(maxSPV)
15deg/secandacaloricasymmetryof10%.Followingthecaloric,patientswereasked,“Didyouhaveanysensationofmotion?”Results:Resultsshowed75%ofpatientsreportedmotionwithameanageof56.51yearscomparedtoameanageof66.55inthe25%ofpatientsreportinganabsenceofmotion.Alogisticregressionwasperformedandtheoverallmodelwasstatisticallysignificantaccountingfor29%ofthevarianceincaloricperception.ThesignificantpredictorvariableswerepatientageandmaxSPVofthecaloricresponse.Theeffectsizeforbothvariableswassmallwithanoddsratioof.9formaxSPVand1.06forage.Conclusions:ThecurrentinvestigationshowedthatbothageandmaxSPVofthecaloricresponseweresignificantpredictorsofvertigoperceptionduringthecaloricexam.However,theassociationbetweenageandcaloricperceptionisnotconclusive.Althoughthereisevidencetosuggestthatthesefindingsrepresentage-relatedchangesinthecentralprocessingofvestibularsystemstimulation,thereareadditionalunmeasuredfactorsthatinfluencetheperceptionofcaloric-inducedvertigo.

简介：Aminoglycosides(AmAn)arewidelyusedfortheirgreatefficiencyagainstgram-negativebacterialinfections.However,theycanalsoinduceototoxichearingloss,whichhasaffectedmillionsofpeoplearoundtheworld.Aspreviouslyreported,individualsbearingmitochondrialDNAmutationsinthe12SrRNAgene,suchasm.1555A>Gandm.1494C>T,aremorepronetoAmAn-inducedototoxicity.Thesemutationscausehumanmitochondrialribosomestomorecloselyresemblebacterialribosomesandenableastrongeraminoglycosideinteraction.Consequently,exposuretoAmAncaninduceorworsenhearinglossintheseindividuals.Furthermore,awiderangeofseverityandpenetranceofhearinglosswasobservedamongfamiliescarryingthesemutations.StudieshaverevealedthatthesemitochondriamutationsaretheprimarymolecularmechanismofgeneticsusceptibilitytoAmAnototoxicity,thoughnuclearmodifiergenesandmitochondrialhaplotypesareknowntomodulatethephenotypicmanifestation.

简介：ObjectiveTodetectearlysignsofnoise-inducedhearingloss(NIHL)inmilitarypilotswithouthearingcomplaints.MethodsPuretoneaudiometryandacousticreflexthresholdsweretestedin36militarypilots(72ears)withnoiseexposurehistorybutnocomplaintsofhearingloss.Conventionaltestfrequencies(0.25-8kHz)andextendedhighfrequencies(EHF,10and12.5kHz)wereincludedinaudiometry.Whitenoiseandpuretonesat0.5,1,2,and4kHzwereusedforacousticreflextests.Twentynormalhearingsubjects(40ears)withnoexposuretooccupationalnoisewereusedascontrols.ResultsPuretonethresholdsatallconventionalfrequenciesandatEHFswereelevatedinthepilots,withthemaximumshiftat4kHz,comparedwithcontrols(p<0.01).ThepilotsalsoshowedelevatedARTtowhitenoiseanddecreaseddifferentialsbetweenwhitenoiseandpuretoneARTs(p<0.01).ConclusionEarlysignsofNIHLarepresentinsomesymptom-freemilitarypilots.Highfrequencyhearingthresholdshift,elevatedwhitenoiseARTanddecreaseddifferentialbetweenwhitenoiseandpuretoneARTsmaybeobjectiveindicatorsofearlyNIHL.

简介：Thereisgrowingevidencesuggeststhatnoise-inducedcochleardamagemayleadtohyperexcitabilityinthecentralauditorysystem(CAS)whichmaygiverisetotinnitus.However,thecorrelationbetweentheonsetoftheneurophysiologicalchangesintheCASandtheonsetoftinnitushasnotbeenwellstudied.Toinvestigatethisrelationship,chronicelectrodeswereimplantedintotheauditorycortex(AC)andsoundevokedactivitiesweremeasuredfromawakeratsbeforeandafternoiseexposure.Theauditorybrainstemresponse(ABR)wasusedtoassessthedegreeofnoise-inducedhearingloss.Tinnituswasevaluatedbymeasuringgap-inducedprepulseinhibition(gap-PPI).Ratswereexposedmonaurallytoahigh-intensitynarrowbandnoisecenteredat12kHzatalevelof120dBSPLfor1h.Afterthenoiseexposure,alltheratsdevelopedeitherpermanent(>2weeks)ortemporary(<3days)hearinglossintheexposedear(s).TheACamplitudesincreasedsignificantly4hafterthenoiseexposure.Mostoftheexposedratsalsoshoweddecreasedgap-PPI.Thepost-exposureACenhancementshowedapositivecorrelationwiththeamountofhearingloss.Theonsetoftinnitus-likebehaviorwashappenedaftertheonsetofACenhancement.

简介：

简介：ObjectiveTostudyeffectsofsaturatedhydrogensalineinpreventingnoise-inducedhearingloss.MethodsFifteenguineapigswererandomlydividedinto3groups(5each),grouponewasforcontrol,grouptwowastreatedwithnormalsalineandgroupthreewastreatedwithsaturatedhydrogensaline,whichwasgivenintraperitoneallyat1hourbeforenoiseexposureat1ml/100g.Onehundredroundsofimpulsenoise(157dBSPLpeak)weredeliveredasnoiseexposure.ImmediatelyafterexposuretoimpulsenoiseandonDays1,2,4and8followingexposure,auditorybrainstemresponse(ABR)thresholdsweremeasured.Outerhaircellmorphologicalchangesandsuccinatedehydrogenase(SDH)activitywereexaminedonDay8post-exposure.ResultsImmediatelyafternoiseexposure,ABRthresholdsinsaturatedhydrogensalinetreatedanimalswerelowerthanthenon-treatedanimals(P<0.05).MicroscopyshowedlittleSDHstaining,cellswellingandirregularcellarrangementinthenon-treatedornormalsalinetreatedanimals.Whereasinthesaturatedhydrogensalinetreatedanimals,therewasdeepSDHstainingwithsignificantlyreducedcelllossandmoreregularcellulararrangementcomparedtotheothertwogroups.Thesurvivingcellscountswas45.17±12.15fornon-treatedanimals,44.50±10.02fornormalsalinetreatedanimalsand,116.50±2.38foranimalstreatedwithsaturatedhydrogensaline.Whilethecountwassimilarbetweennon-treatedandnormalsalinetreatedanimals,itwassignificantlyhigherinsaturatedhydrogensalinetreatedanimals(P<0.05).ConclusionsIntraperitonealinjectionofsaturatedhydrogensalineappearstoprotectthecochleaagainstnoise-induceddamage.

简介：Objective:Toidentifypresenceofinflammasomeactivatedinmousecochleawithsensorineuralhearingloss(SNHL)causedbycytomegalovirus(CMV)infection.Method:MCMVwasinjectedintotherightcerebralhemisphereinneonatalBALB/cmiceat2000pfuvirustiters.Auditorybrainstemresponses(ABRs)weretestedtoevaluatehearingat21days.HistopathologicalstudieswereconductedtoconfirmlocalizationsofMCMVinfectedcellsintheinnerear.Expressionofinflammasomerelatedfactorswasassessedbyimmunofluorescence,Quantitativereal-timePCRandWesternblotting.Results:InthemousemodelofCMVinducedSNHL,inflammasomerelatedkinaseCaspase-1anddownstreaminflammatoryfactorIL-1bandIL-18werefoundincreasedandactivatedafterCMVinfectioninthecochlea.Thesefactorscouldfurtherup-regulateexpressionofIL-6andTNFa.Theseinflammatoryfactorsareneurotoxicityandmaycontributetohearingimpairment.Furthermore,wealsodetectedsignificantlyincreasedAIM2proteinthataccumulatedintheSGNofcochleaewithCMVinfection.Significance:Wehaveshownthatinflammasomeasanovelinherentimmunitymechanismmaycontributetohearingimpairment.Conclusion:OurdataindicatethatimflammasomeassembleinmouseinnerearinresponsetoCMVinfection.WehaverevealedanovelpathologyeventinCMVinducedSNHLinvolvingactivationofinflammasomeinmousecochlea.Additionally,wehaveshownthatinflammasomemaybeanoveltargetforpreventionandtreatmentofCMVrelatedSNHL.

简介：ObjectiveTounderstandthemechanismofnoiseexposureinducedouterhaircells(OHCs)deathpathways.MethodsThirtytwoguineapigswereusedinthisstudy.Theanimalswereeitherexposedfor4h/daytobroadbandnoiseat122dBSPL(A-weighted)for2consecutivedaysorperfusedwithMNNG.Afterauditorytest,thecochleaeofanimalsweredissected.Propidiumiodide(PI),aDNAintercalatingfluorescentprobe,wasusedtotracemorphologicalchangesinOHCnuclei.F-actinstainingwasusedtodeterminemissingOHCs.Caspase-3wasdetectedinlivingorganofCortiwholemountsusingthefluorescentprobe.ThesinglestrandDNA(ssDNA)inapoptoticOHCsinguineapigsandapoptosisinducingfactor(AIF)inhaircellsinguineapigswereexaminedbyimmunohistologymethod.WholemountsoforganofCortiwereprepared.Morphologicalandfluorescentchangeswereexaminedunderaconfocalmicroscope.Results(1)Bothapoptoticandnecrotichaircellsappearedfollowingnoiseexposure.(2)NoiseexposureinducedsinglestrandDNAinapoptoticOHCsbutnotinthenormalOHCs.(3)EitherafternoiseexposureorafterMNNGperfusion,apoptoticOHCswerefeaturedbynuclearcondensationorfragmentationwithcaspase-3activation,whereasnecroticOHCswerecharacterizedbynuclearswellingwithoutcaspase-3activation.(4)InnormalorganofCorti,AIFwaslocatedinthemitochondriaareas.Afternoiseexposure,AIFwastranslocatedfrommitochondriainapoptoticandnecroticOHCs.ConclusionThesefindingsindicatethatnoiseexposuredamagesDNAintheOHC,whichtriggersactionofCaspase-3.Subsequently,AIFistranslocatedtothenucleus,leadingtoDNAdamageandOHCsdeath.

简介：Hearingloss(HL)isoneofthemostwidespreadsensorydisorders,affectingapproximately1in500newborns.HeritablediseasesoftheinnereararetheleadingcausesofprelingualHL.TreatingofhereditaryHLandunderstandingitsunderlyingmechanismsremaindifficultchallengestootolaryngologists.Asstemcellsarecapableofself-renewalanddifferentiation,theyareideallysuitedbothfordiseasemodelingandregenerativemedicine.Recently,descriptionofinducedpluripotentstemcells(iPSCs)hasallowedthefieldofdiseasemodelingandpersonalizedtherapytobecomefarmoreaccessibleandphysiologicallyrelevant,asiPSCscanbegeneratedfrompatientsofanygeneticbackground.ThisreviewbrieflydescribestheadvantagesofiPSCstechnologyanddiscussespotentialapplicationsofthispowerfulbiologicaltoolinstudyingandtreatinghereditaryHL.

简介：BackgroundChronicotitismedia(COM)isasignificantclinicalproblem.UnderstandingthemechanismsofCOMiscriticalforitscontrolandtreatment.However,littleisknownoftheprocessesleadingtoCOMasaresultoflackofanimalmodelsofN-ethyl-N-nitrosourea(ENU)inducedmutationsinotitismediawitheffusion(OME).MethodsOtoscopyandauditorybrainresponse(ABR)evaluationwerecarriedoutundersedationinNmf391nmf/nmfmiceof2,4,6and8monthsofage.Themicewerekilledforstudyofmiddleandinnerearpathology.ResultsTympanicmembranevisualizationandABRthresholdsin1-to8-month-oldNmf391nmf/nmfmiceshowedspontaneousOMEandinnereardiseasesinapproximately100%oftheanimals.ThesignificantelevationofABRthresholdssuggestedasensorineuralcomponentinhearinglossinadditiontotheconductiveloss.Middleandinnerearhistologyshowedvariousdegreesofouterhaircellslossandmiddleearinflammationinallthemice,butnoinflammationcellsintheinnerear.TheABRthresholdat32kHzwassignificantlyelevated.ConclusionsThisstudyshowshistopathologicchangesintheNmf391nmf/nmfmousemodelofCOMwitheffusionthathavenotbeenreportedinhumanCOM.ThisENUinducedmutationmodelofCOMwillbevaluableforthecharacterizationofmiddleearinflammationandinnereardiseaseprocessesthatareinducedbymiddleearinfections.WeproposethatCOMwitheffusioninthisENUinducedmutationmodelisthecauseofthecochleahaircellsdamage.

简介：TheLy5.1mouse,alsotermedB6.SJL-PtprcaPepcb/BoyJ,isacongenicstrainwidelyusedasarecipientinanimalstudiesofbonemarrowtransplant.OurpreviousstudydocumentedthatamajorityoftypeIspiralganglionneurons(SGNs)intheapicalturnsofLy5.1miceareunmyelinatedandaggregateintoneuronalclusters,similartothespiralganglioninthehumanear.Ouabain,awellknownNa-KATPaseinhibitor,hasbeenshowntoinduceneuronaldegenerationinavarietyofneuraltissuesincludingtheadultgerbilandCBA/CaJmousespiralganglion.Here,functionalandpathologicalchangesoftheauditorynervesinyoung-adultLy5.1micewereexaminedat3,7and14daysafterouabainexposure.SimilartoobservationsinCBA/CaJmice,ouabainapplicationselectivelyremovedtypeISGNs,resultinginanimmensedeclineoftheauditorynervefunction.Hyperplasiaofglialcellswasseenintheinjuredauditorynervesat7daysafterouabainexposure.Ourdataindicatethatthe'human-like'featuresofunmyelinatedtypeISGNshavenoprotectiveimpactonthefateofSGNsafterouabainexposure.Cellsincorporatingbromodeoxyuridine(BrdU)andexpressingSox2werealsocountedintheauditorynervesofcontrolandouabain-treatedears.ThenumberofSox2+glialcellssignificantlyincreasedat3and7dayspost-treatment.Interestingly,thehighestdensityofBrdU+cellsappearedintheapicalturnoftheinjuredauditorynerveshortlyafterouabainexposure,suggestingthatthepatternofSGNlossattheapicalturninLy5.1mousemayhavesomeimpactonthereactionofnon-neuronalcellsinresponsetoacuteototoxicdrugexposureintheauditorynerve.

简介：ObjectiveToinvestigatetheoccurrenceandpossiblemechanismsofapoptosisincochlearepitheliumandspiralganglionneuronsaftermefloquinetreatment.MethodsWeusedquantitativeRT-PCRapoptosis-focusedgenearrays(96-well,84apoptosisrelatedgenes)toassesschangesofgeneexpressioninthecochlearbasilarmembrane(haircells-supportingcells)andspiralganglionneuronsofratcochlearorganotypicculturestreatedwith100μMmefloquinefor3h.ResultsSignificantup-ordown-regulationingeneexpressionwasdetectedin23genesinthecochlearbasilarmembrane,andin32genesinthespiralganglionneuronscomparedwithtime-matchedcontrols.Therespondinggenescouldbeclassifiedaspro-oranti-apoptotic,andweremainlyimplicatedintheBcl-2,Caspase,Card,IAP,TNFligand/TNFreceptor,Deathdomain/Deatheffectordomain,DNAdamage/p53,andNF-kappaBfamilies.Syntheticanalysissuggestedthatthesefamiliescouldberevisedtotwomajorpathwaysmainlyinvolvedinthedeathreceptor-mediatedsignalingpathwayandapoptoticmitochondrialpathway.Inaddition,itwasfoundthatnumerousanti-apoptoticgenessuchasBcl2a1,Birc1b,Birc3,Birc4,Bnip1,Cflar,Il10,Lhx4,Mcl1,Nfkb1,Prlr,Prok2,andTNFweregreatlyup-regulatedinthecochleartissue,whichmightimplytheco-existenceofprotectiveresponseinthecellsattheearlystageofmefloquine-induceddamage.

简介：ObjectiveThisstudyistoexploretherelationshipbetweenacetylcholine(ACh)-inducedcalciumreleasefromintracellularCa2+storesandfunctionofouterhaircell(OHC)motors,inanattempttoelucidatethemechanismofOHCelectromotilityatrestingstate.MethodsOHCswereisolatedfromadultguineapig(200-300g)cochleaandloadedwithFluo-3/AM.ThecellsweretreatedwithACh/dHBSS,ACh/HBSS,dHBSSonlyorHBSSonly.Intracellular[Ca2+]ivariationsincellsunderthefourtreatmentswereobservedusinganAr-Krlaserscanconfocalmicroscope.Results[Ca2+]ioscillationswererecordedinfiveOHCstreatedwithACh/dHBSSbutnotinothercells.ThisisthefirsttimethatAch-excited[Ca2+]ioscillationsarereportedinguineapigOHCsindependentofextracellularcalcium.ConclusionsACh-excited[Ca2+]ioscillationsinOHCsoriginatesfromintracellularcalciumreleaseandmayplayacrucialroleinmaintainingactivemechanicalmotilityoftheOHCatrestingandmodulatingOHCelectromotility.

简介：Hearinglossandtinnitusareamongthemostcommonconsequencesoflongtermnoiseexposureandre-mainanunder-addressedheathissueinmostdevelopingnationsincludingChina.Therapidindustrializa-tionandlifestylechangesinChinaincreasetheconcernovernoiseexposureandnoiseinducedhearingloss(NIHL).ResearchonNIHLinChinaislimited.ThecurrentpaperreviewsstudiespublishedinEnglishandChineselanguageliteraturesregardingnoiseexposureandNIHLinChina.TheirimplicationontheChi-nesepopulationisdiscussed.ThepossibleutilityofaresearchmodelsuchastheDangerousDecibels?asameanstoincreaseunderstandingofthescopeofNIHLamongtheChinesepopulation,toeducatethegener-alpublicinChina(especiallytheyoung)aboutNIHLanditsprevention,andtostudyeffectsoflanguageandculturalfactorsoninternationalinformationdisseminationandbehavioralinterventionsisproposed.

简介：Cisplatinbelongstoplatinum-baseddrugsandiswidelyusedincancerchemotherapy.Ototoxicityisoneofthemajordoselimitingside-effectsofcisplatin.Fortoxicitytooccurcisplatinmustfirstbetransportedfromthebloodstreamintocochlearcells.Threecoppertransportersareconsideredpathwaysforregulatingtheuptakeandtranslocationofcisplatinintocells:Ctr1,ATP7AandATP7B.Ourrecentstudywithcochlearorganotypicculturesshowsthatcochlearhaircellscanbedestroyedbycisplatinatlowconcentrationsfrom10μmto100μn.However,highdosesofcisplatincannotdamagehaircells,maybeduetointrinsicfeedbackreactionsthatincreaseexportofplatinumbyATP7Bwhentheplatinumconcentrationishighinextracellularspace.Cimitidineisaspecificcoppertransporterinhibitorthatcanblocktheentranceofcopperandplatinum,andmaypreventcisplatin-inducedcochlearhaircellinjury.Toevaluatethishypothesis,wetreatedcochlearorganotypiccultureswithcisplatin(10μmor50μm)alone,orcisplatincombinedwithcimitidineatconcentrationsrangingfrom10-2000μmfor48hours.cisplatinat10μmdamagedabout20%haircells.Incontrast,whencimitidine(10μm,100μmand2000μm)wasaddedtotheculture,near100%cochlearhaircellsurvived.Athigherconcentration(50μm),cisplatindestroyedabout80%ofcochlearhaircells.However,100μmcimitidinerescuedabout50%haircellsfromcisplatindamage,and2000μmcimitidineprotectedabout80%haircells.ThedataofwesternblotshowedthatCTR1andATP7Bexpressionswereincreasedincisplatintreatedcochleartissue,butcimitidinesignificantlyreducedCTR1andATP7B.Inaddition,ATP7Aexpressionwasdepressedalittleaftercisplatintreatment.ConsideringthatCtr1isinvolvedincopperandplatinuminflux,buttheATP7AandATP7Barecopperexporttransporters,theresultssuggestthatcimitidinecaneffectivelyblocktheentrancebycoppertransportersandstoptheinfluxofcisplatin.

简介：Cisplatin,awidelyusedanticancerdrug,damageshaircellsincochlearorganotypicculturesatlowdoses,butparadoxicallycauseslittledamageathighdosesresultinginaU-shapeddose-responsefunction.Todetermineifthecisplatindose-responsefunctionforvestibularhaircellsfollowsasimilarpattern,wetreatedvestibularorganotypiccultureswithdosesofcisplatinrangingfrom10to1000μM.Vestibularhaircelllesionsprogressivelyincreasedasthedoseofcisplatinincreasedwithmaximumdamageoccurringaround50–100μM,butthelesionsprogressivelydecreasedathigherdosesresultinginlittlehaircelllossat1000μM.TheU-shapeddoseresponsefunctionforcisplatin-treatedvestibularhaircellsincultureappearstoberegulatedbycoppertransporters,Ctr1,ATP7AandATP7B,thatdose-dependentlyregulatetheuptake,sequestrationandextrusionofcisplatin.

简介：Thewaltzingguineapigmaybeagoodmodeltoinvestigateifgeneticfactorcanchangethesensitivityinnoise-inducedhearingloss.Atotalof34waltzigguineapigswerestudiedandwefoundthatthereisnoanysignificantincreasedsensitivitytonoisetraumaiftheage-inducedhearinglosswasconsideredinwaltz-ingguineapig.

简介：ObjectiveToestablishananimalmodelofsuddenonsetsensorineuralhearingloss(SSNHL)tostudyitsmechanisms.MaterialsandmethodsTheinnerearwasexposedto3-nitropropionicacidat0.5mol/L(3-NP(H))and0.3mol/L(3-NP(L))throughtheroundwindowmembranefor30minutesin50maleguineapigs.Thresholdsofauditorybrainstemresponses(ABR)wereestablishedbeforethetreatmentandretestedat4hours,1day,3daysand6daysfollowing3-NPexposure.Controlanimalsweretreatedwithphosphatebufferedsaline(PBS)andtheirABRswereretestedat4hoursand1dayafterthetreatment.Animalsweremonitoredfornystagmusandposturalsignsofvestibulardysfunction,usingadigitalvideocamera,followingthetreatmentprocedure.Specimensweretakenat12hours,1day,3daysand7daysfollowing3-NP(H)exposureandembeddedinJB4forlightmicroscopyobservation.ResultsABRswerelostinallanimalstestedat4hoursfollowing3-NP(H)exposure.TherateofcompleteABRlossdecreasedaspost-treatmenttesttimeincreased.ABRswerelostin80%(4/5)oftheanimalsat1dayafterexposureto3-NP(L).Spontaneoushorizontalnystagmuswithafastphaseawayfromthetreatedeardevelopedinall3-NP(H)-treatedanimalsandin20%(1/5)oftheanimalsexposedto3-NP(L),exceptfortheonetreatedbilaterally.Variousdegreeofposturaldisturbancesconsistentwithunilateralvestibulardysfunction,suchasspontaneousbarrelrollingtowardstheexposuresidewhilewalking,wereseeninallanimalsexposedto3-NP(H)and40%(2/5)ofanimalsexposedto3-NP(L),exceptfortheoneanimaltreatedbilaterally,whichshowednosignsofimbalance.Bothnystagmusandposturaldisturbancesresolvedin2daysfollowing3-NPexposure.HistologicalstudyshowedtemporaryedematintheorganorCorti,Claudiuscellsandtheinnersulcuscells3daysafter3-NP(H)treatment.Enlargementofintercellularspaceinthespiralprominencewasfirstnoticedat12hourspost-3-NP(H)exposure,progressedatd

简介：Noise-inducedhearinglossisacommoncauseofacquiredhearinglossintheadultpopulation.Acousticoverstimulationcausescochleardamagethroughmechanicalstresstothetissue.Consequently,complexmolec-ularchangesareinitiated,andthesechangesleadtomorphologicalandbiologicalalterationsinthecochlea,whichinturncompromisethecochlearfunctionandcausehearingloss.Inthepast10years,therehavebeensignificantadvancesinourunderstandingofthemolecularmechanismsofnoise-inducedhearingloss.Theseadvancesareattributed,inpart,tothedevelopmentofhigh-throughputtechnologiesfortheglobalanalysesofmolecularchanges.Inthisreview,webrieflydescribethenewlydevelopedmethodsforinvestigatingthemo-lecularresponsesofthecochleatoacoustictraumaandtheknowledgegeneratedfromthesestudies.Wealsodiscussthestrengthsandlimitationsofeachtechniqueandthemajorchallengestoinvestigatecochleardegen-erationfollowingacousticinjury.