ObjectiveTostudygentamicininjurymechanismsusingpostnatalmousecochlearspiralgangcells(SGC).MethodsSGCswereisolatedusingacombinatorialapproachofenzymaticdigestionandmechanicalseparationfromP2~6Kunmingmousecochleae.After4days,culturedSGCswerefixedwith4%paraformaldehydeatroomtemperatureforimmunocytochemicalexaminationusingthemethodsofS-Pandthemonoclonalantibodyagainstmouseneurofilamentprotein(Neurofilament-68/200Kda,NF-L+H).SGCswererandomlypidedintoablankcontrolgroupandthreegentamicintreatmentgroups(mediumgentamicinconcentrationat50mg/L,100mg/Land150mg/Lrespectively),SGCswerecollectedandexaminedunderatransmissionelectronmicroscopeafterbeingculturedfor48h.ResultsSGCprimaryculturewassuccessful.SGCcytoplasmandneuritesweredyedbrownishyellowbythemonoclonalmouseneurofilamentproteinantibody.SGCsshowedclassicalbipolarneuronappearance.Underthetransmissionelectronmicroscope,.gentamicintreatedSGCsshowedmorphologicalfeaturesdifferentcomparedtothoseintheblankcontrolgroup,whichmightindicateapoptosis.ConclusionOurresultsindicatethatgentamicinhasdirecttoxiceffectsoncochlearSGCsinmiceandtheinjurymechanismiscloselyrelatedwithapoptosis.Damagetomitochondriamayplayanimportantroleintheprocess.