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1、英文论文投稿信Coverletter模板Case1DearEditor,Wewouldliketosubmittheenclosedmanuscriptentitled"GDNFAcutelyModulatesNeuronalExcitabilityandA-typePotassiumChannelsinMidbrainDopaminergicNeurons",whichwewishtobeconsideredforpublicationinNatureNeuroscience.GDNFhaslongbeenthoughttobeapotentne
2、urotrophicfactorforthesurvivalofmidbraindopaminergicneurons,whicharedegeneratedinParkinson’sdisease.Inthispaper,wereportanunexpected,acuteeffectofGDNFonA-typepotassiumchannels,leadingtoapotentiationofneuronalexcitability,inthedopaminergicneuronsincultureaswellasinadultbrainsli
3、ces.Further,weshowthatGDNFregulatestheK+channelsthroughamechanismthatinvolvesactivationofMAPkinase.Thus,thisstudyhasrevealed,forthefirsttime,anacutemodulationofionchannelsbyGDNF.OurfindingschallengetheclassicviewofGDNFasalong-termsurvivalfactorformidbraindopaminergicneurons,an
4、dsuggestthatthenormalfunctionofGDNFistoregulateneuronalexcitability,andconsequentlydopaminerelease.TheseresultsmayalsohaveimplicationsinthetreatmentofParkinson’sdisease.Duetoadirectcompetitionandconflictofinterest,werequestthatDrs.XXXofHarvardUniv.,andYYofYaleUniv.notbeconside
5、redasreviewers.Withthanksforyourconsideration,IamSincerelyyours,case2DearEditor,Wewouldliketosubmittheenclosedmanuscriptentitled"Ca2+-bindingproteinfrequeninmediatesGDNF-inducedpotentiationofCa2+channelsandtransmitterrelease",whichwewishtobeconsideredforpublicationinNeuron.Web
6、elievethattwoaspectsofthismanuscriptwillmakeitinterestingtogeneralreadersofNeuron.First,wereportthatGDNFhasalong-termregulatoryeffectonneurotransmitterreleaseattheneuromuscularsynapses.Thisprovidesthefirstphysiologicalevidenceforaroleofthisnewfamilyofneurotrophicfactorsinfunct
7、ionalsynaptictransmission.Second,weshowthattheGDNFeffectismediatedbyenhancingtheexpressionoftheCa2+-bindingproteinfrequenin.Further,GDNFandfrequeninfacilitatesynaptictransmissionbyenhancingCa2+channelactivity,leadingtoanenhancementofCa2+influx.Thus,thisstudyhasidentified,forth
8、efirsttime,amoleculartargetthatmediatesthelong-term,synaptica
