Ca2+ Permeable AMPA Receptor Induced Long-Term Potentiation Requires PI3MAP Kinases but Not CaCaM-Dependent Kinase II 英文参考文献.docVIP

下载本文档

4
0
约5万字
约 14页
2017-05-11 发布于上海
举报
版权申诉

Ca2+ Permeable AMPA Receptor Induced Long-Term Potentiation Requires PI3MAP Kinases but Not CaCaM-Dependent Kinase II 英文参考文献.doc

1、原创力文档（book118）网站文档一经付费（服务费），不意味着购买了该文档的版权，仅供个人/单位学习、研究之用，不得用于商业用途，未经授权，严禁复制、发行、汇编、翻译或者网络传播等，侵权必究。。
2、本站所有内容均由合作方或网友上传，本站不对文档的完整性、权威性及其观点立场正确性做任何保证或承诺！文档内容仅供研究参考，付费前请自行鉴别。如您付费，意味着您自己接受本站规则且自行承担风险，本站不退款、不进行额外附加服务；查看《如何避免下载的几个坑》。如果您已付费下载过本站文档，您可以点击这里二次下载。
3、如文档侵犯商业秘密、侵犯著作权、侵犯人身权等，请点击“版权申诉”（推荐），也可以打举报电话：400-050-0827(电话支持时间：9:00-18:30)。
4、该文档为VIP文档，如果想要下载，成为VIP会员后，下载免费。
5、成为VIP后，下载本文档将扣除1次下载权益。下载后，不支持退款、换文档。如有疑问请联系我们。
6、成为VIP后，您将拥有八大权益，权益包括：VIP文档下载权益、阅读免打扰、文档格式转换、高级专利检索、专属身份标志、高级客服、多端互通、版权登记。
7、VIP文档为合作方或网友上传，每下载1次，网站将根据用户上传文档的质量评分、类型等，对文档贡献者给予高额补贴、流量扶持。如果你也想贡献VIP文档。上传文档

Ca2PermeableAMPAReceptorInducedLong-TermPotentiationRequiresPI3MAPKinasesbutNotCaCaM-DependentKinaseII英文参考文献

Ca2+PermeableAMPAReceptorInducedLong-Term PotentiationRequiresPI3/MAPKinasesbutNotCa/CaM- DependentKinaseII SuhailAsrar1,2,ZikaiZhou1,2,WeiRen3,ZhengpingJia1,2* 1NeurosciencesandMentalHealth,HospitalforSickChildren,Toronto,Ontario,Canada,2DepartmentofPhysiology,UniversityofToronto,Toronto,Ontario,Canada, 3CollegeofLifeScience,ShaanxiNormalUniversity,Xi’an,China Abstract Ca2+ influx via GluR2-lacking Ca2+-permeable AMPA glutamate receptors (CP-AMPARs) can trigger changes in synaptic efficacyinbothinterneuronsandprincipleneurons,buttheunderlyingmechanismsremainunknown.Wetookadvantage ofgeneticallyalteredmicewithnoorreducedGluR2,thusallowingtheexpressionofsynapticCP-AMPARs,toinvestigate the molecular signaling process during CP-AMPAR-induced synaptic plasticity at CA1 synapses in the hippocampus. Utilizingelectrophysiologicaltechniques,wedemonstratedthatthesereceptorswerecapableofinducingnumerousforms of long-termpotentiation (referred toas CP-AMPAR dependentLTP) through anumberof different inductionprotocols, includinghigh-frequencystimulation(HFS)andtheta-burststimulation(TBS).Thisincludedapreviouslyundemonstrated form of protein-synthesis dependent late-LTP (L-LTP) at CA1 synapses that is NMDA-receptor independent. This form of plasticity was completely blocked by the selective CP-AMPAR inhibitor IEM-1460, and found to be dependent on 2+ postsynapticCa ionsthroughcalciumchelator(BAPTA)studies.Surprisingly,Ca/CaM-dependentkinaseII(CaMKII),thekey proteinkinasethatisindispensableforNMDA-receptordependentLTPatCA1synapsesappearedtobenotrequiredforthe induction of CP-AMPAR dependent LTP due to the lack of effect of twoseparate pharmacological inhibitors (KN-62 and staurosporine) onthisformofpotentiation.BothKN-62andstaurosporinestronglyinhibitedNMDA-receptordependent LTPincontrolstudies.Incontrast,inhibitorsforPI3-kinase(LY294002andwortmannin)ortheMAPKcascade(PD98059and U0126)significantlyattenuatedthisCP-AMPAR-dependentLTP.Similarly,postsynapticinfusionoftetanustoxin(