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NEURALREGENERATIONRESEARCHVolume7,Issue16,June2012Citethisarticleas:NeuralRegenRes.2012;7(16):1234-1240.1234JufangHuang☆,M.D.,Researcher,DepartmentofAnatomyandNeurobiology,XiangyaSchoolofMedicine,CentralSouthUniversity,Changsha410013,HunanProvince,ChinaCorrespondingauthor:DanChen,M.D.,Lecturer,DepartmentofAnatomyandNeurobiology,XiangyaSchoolofMedicine,CentralSouthUniversity,Changsha410013,HunanProvince,Chinadannychen0101@yahoo.com.cnReceived:2012-02-22Accepted:2012-05-03(N20111028002/H)HuangJF,ZhouLH,WangH,LuoJ,XiongK,ZengLP,ChenD.Spatiotemporalalterationsofpresynapticelementsintheretinaafterhighintraocularpressure.NeuralRegenRes.2012;7(16):1234-1240.www.crter.cnwww.nrronline.orgdoi:10.3969/j.issn.1673-5374.2012.16.005Spatiotemporalalterationsofpresynapticelementsintheretinaafterhighintraocularpressure****☆JufangHuang,LihongZhou,HuiWang,JiaLuo,KunXiong,LepingZeng,DanChenDepartmentofAnatomyandNeurobiology,XiangyaSchoolofMedicine,CentralSouthUniversity,Changsha410013,HunanProvince,ChinaAbstractAratmodelofacutehighintraocularpressurewasestablishedbyinjectingsalineintotheanteriorchamberofthelefteye.Synaptophysinexpressionwasincreasedintheinnerplexiformlayerat2hoursfollowinginjury,andwaswidelydistributedintheouterplexiformlayerat3–7days,andthendecreasedtothenormallevelat14days.Thissuggeststhatexpressionofthispresynapticfunctionalproteinexperiencedspatiotemporalalterationsafterelevationofintraocularpressure.Therewasnosignificantchangeinthefluorescenceintensityanddistributionpatternforsynapse-associatedprotein102followingelevatedintraocularpressure.Synapse-associatedprotein102immunoreactivitywasconfinedtotheouterplexiformlayer,whilesynaptophysinimmunoreactivityspreadintotheouterplexiformlayerandtheouternuclearlayerat3and7daysfollowinginjury.Thesealterationsinpresynapticelementswerenotaccompaniedbychangesinpostsynapticcomponents.KeyWordssynaptophysin;synapse-associatedprotein102;synapticplasticity;elevatedintraocularpressure;retina;neuralregenerationAbbreviationsSYN,synaptophysin;SAP102,synapse-associatedprotein102;IPL,innerplexiformlayer;OPL,outerplexiformlayer;HIOP,highintraocularpressureINTRODUCTIONThemorphologicchangesinsynapsesandthemodulationofthestrengthorefficacyofsynapticsignalingarecommonlyknownassynapticplasticity.Synapticplasticity,whichplaysanimportantroleinthedevelopmentofsynapticconnectionsandinthefunctioningofthematurenervoussystem,isdependentonpresynapticaswellaspostsynapticchanges.Synaptophysin(SYN),alsoknownasP38,isanacidiccalciumbindingglycoproteincloselyassociatedwithsynapticstructureandfunction,andisanintegralmembraneproteinofsynapticvesicles[1].SYNiswidelyusedasamarkerofsynaptogenesisandpresynapticterminals[2-3].Synapse-associatedprotein102(SAP102)isamemberofthemembrane-associatedguanylatekinaseproteinfamily,andisenrichedinpostsynapticdensitiesandisinvolvedinreceptor-mediatedsynaptictransmission.SAP102iscrucialfortheregulationofsynapticsignalingandplasticity[4-5].Intheratretina,synapsesintheouterandinnerplexiformlayers(OPLandIPL)playanimportantroleinvisualsignaltransmission[6].Studiesonsynapticchangesintheseregionsfollowinginjurymayprovidesignificantinsightintopathogeneticandprotectivemechanismsineyediseasessuchasglaucoma.Elevationofintraocularpressure(IOP)isariskfactorforglaucoma.Previousstudieshaveshownthatacutehighintraocularpressure(HIOP)causesthin...