摘要
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.
出版日期
2014年03月13日(中国期刊网平台首次上网日期,不代表论文的发表时间)