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1、DearEditor,Wewouldliketosubmittheenclosedmanuscriptentitled"GDNFAcutelyModulatesNeuronalExcitabilityandA-typePotassiumChannelsinMidbrainDopaminergicNeurons",whichwewishtobeconsideredforpublicationinNatureNeuroscience.GDNFhaslongbeenthoughttobeapotentn
2、eurotrophicfactorforthesurvivalofmidbraindopaminergicneurons,whicharedegeneratedinParkinson’sdisease.Inthispaper,wereportanunexpected,acuteeffectofGDNFonA-typepotassiumchannels,leadingtoapotentiationofneuronalexcitability,inthedopaminergicneuronsincul
3、tureaswellasinadultbrainslices.Further,weshowthatGDNFregulatestheK+channelsthroughamechanismthatinvolvesactivationofMAPkinase.Thus,thisstudyhasrevealed,forthefirsttime,anacutemodulationofionchannelsbyGDNF.OurfindingschallengetheclassicviewofGDNFasalon
4、g-termsurvivalfactorformidbraindopaminergicneurons,andsuggestthatthenormalfunctionofGDNFistoregulateneuronalexcitability,andconsequentlydopaminerelease.TheseresultsmayalsohaveimplicationsinthetreatmentofParkinson’sdisease.Duetoadirectcompetitionandcon
5、flictofinterest,werequestthatDrs.XXXofHarvardUniv.,andYYofYaleUniv.notbeconsideredasreviewers.Withthanksforyourconsideration,IamSincerelyyours,case2DearEditor,Wewouldliketosubmittheenclosedmanuscriptentitled"Ca2+-bindingproteinfrequeninmediatesGDNF-in
6、ducedpotentiationofCa2+channelsandtransmitterrelease",whichwewishtobeconsideredforpublicationinNeuron.WebelievethattwoaspectsofthismanuscriptwillmakeitinterestingtogeneralreadersofNeuron.First,wereportthatGDNFhasalong-termregulatoryeffectonneurotransm
7、itterreleaseattheneuromuscularsynapses.Thisprovidesthefirstphysiologicalevidenceforaroleofthisnewfamilyofneurotrophicfactorsinfunctionalsynaptictransmission.Second,weshowthattheGDNFeffectismediatedbyenhancingtheexpressionoftheCa2+-bindingproteinfreque
8、nin.Further,GDNFandfrequeninfacilitatesynaptictransmissionbyenhancingCa2+channelactivity,leadingtoanenhancementofCa2+influx.Thus,thisstudyhasidentified,forthefirsttime,amoleculartargetthatmediatesthelong-term,synapticactionofaneurotrophicfacto