407ActaPhysiologicaSinica,October25,2006,58(5):407-414http://www.actaps.com.cnResearchPaperReceived2006-06-15Accepted2006-08-09ThisworkwassupportedtheNationalBasicResearchPrioritiesProgrammeofChina(No.2005CB724301)andtheMinistryofEducationofChina(No.20040248062).*Correspondingauthor.Tel:+86-21-34204015;Fax:+86-21-34204016;E-mail:pjliang@sjtu.edu.cn**Presentaddress:ComputerScienceDepartment,BlueSkyVocationalandTechnicalInstitute,Nanchang330029,China.Postsynapticcalciumpathwaycontributestosynapticplasticitybetweenretinalconesandluminosity-typehorizontalcellsHUANGShi-Yong1,HUJian-Feng1,**,GONGHai-Qing2,LIANGPei-Ji2,*1ShanghaiInstitutesforBiologicalSciences,ChineseAcademyofSciences,Shanghai200031,China;2DepartmentofBiomedicalEngineering,ShanghaiJiaotongUniversity,Shanghai200240,ChinaAbstract:Itwaspreviouslyfoundthattheefficacyofsynaptictransmissionbetweenretinalconesystemsandluminosity-typehorizontalcells(LHCs)wasactivity-dependent.Repetitiveactivationofred-conepathwayincreasedtheLHC’shyperpolarizingresponsetoredlight,andtheresponseenhancementwasreversible.Inthisstudy,intracellularrecordingandpharmacologicalmethodwereappliedtoinvestigatethemechanism(s)underlyingred-flickering-inducedresponseenhancement.LoweringintracellularCa2+intheLHCbyintracellularinjectionofCa2+chelatorEGTApreventedthedevelopmentofred-flickering-inducedresponseenhancement,whichimplicatestheimportanceofpostsynapticcalciumsignal.TheresponseenhancementcouldalsobeeliminatedbyapotentantagonistofCa2+-permeableAMPAreceptor(CP-AMPAR),whichsuggeststhepossibilitythatCa2+influxviaglutamate-gatedcalciumchannelsisrelatedtothechangesof[Ca2+]i.Furthermore,theadministrationofryanodineorcaffeinealsoattenuatedthephenomenon,whichgivesevidencethatthelocalcalciumsignalcausedbyintracellularcalcium-inducedcalciumrelease(CICR)maybeinvolved.Takentogether,ourdataimplicatethatpostsynapticCICRandCP-AMPARarerelatedtotheactivity-dependentresponseenhancement.Keywords:AMPA;calcium;neuronalplasticity;retina;ryanodinereceptor/calciumreleasechannel突触后钙通路有助于视锥与L型水平细胞间的突触可塑性黄仕勇1，胡剑锋1,**，龚海庆2，梁培基2,*1中国科学院上海生命科学研究院，上海200031；2上海交通大学生物医学工程系，上海200240摘要：我们实验室以前发现，视网膜视锥与亮度型水平细胞(luminosity-typehorizontalcell,LHC)之间的突触传递效率具有可塑性。重复性刺激红敏视锥增加了LHC对红光的超极化反应幅度，而且这种增强作用是可逆的。在本文中，我们运用细胞内记录技术和药理学分析的方法来考察重复性红光刺激引起的反应增强的可能机制。当通过胞内注射Ca2+的螯合剂EGTA来降低LHC内的Ca2+浓度后，重复性红光引起的反应增强被抑制，提示突触后钙信号是反应增强的一个重要因素。另外，反应增强现象还可以被钙离子通透的AMPA受体(Ca2+-permeableAMPAreceptor,CP-AMPAR)的拮抗剂阻断，说明通过钙离子通透的谷氨酸受体内流的Ca2+与胞内Ca2+浓度的改变有关。进一步发现，胞外灌流ryanodine或caffeine也可以消除反应增强现象，说明由钙诱导的钙释放(calcium-inducedcalciumrelease,CICR)引起的钙信号可能也参与了反应增强现象的产生。结果提示，CICR和CP-AMPAR与重复性红光刺激引起的LHC对红光的反应增强有关。关键词：AMPA；钙离子；神经元可塑性；视网膜；ryanodine受体/钙释放通道中图分类号：Q436ActaPhysiologicaSinica,October25,2006,58(5):407-414408Intheouterplexiformlayerofthecarpretina,luminosity-typehorizontalcell(LHC)playsanimportantroleinvisualsignalprocessing.Itreceivessynapticinputfrombothred-andgreen-sensitiveconesthattonicallyr...
