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1、16530•TheJournalofNeuroscience,November14,2012•32(46):16530–16538Cellular/MolecularSerotoninActivatesCatecholamineNeuronsintheSolitaryTractNucleusbyIncreasingSpontaneousGlutamateInputsRanJiCui,*BrandonL.Roberts,*HuanZhao,MingyanZhu,andSuzanneM.AppleyardPrograminNeuroscience,Departme
2、ntofVeterinaryComparativeAnatomy,PhysiologyandPharmacology,WashingtonStateUniversity,Pullman,Washington99164Serotonin(5-HT)isacriticalneurotransmitterinthecontrolofautonomicfunctions.5-HT3receptorsparticipateinvagalafferentfeedbacktodecreasefoodintakeandregulatecardiovascularreflexe
3、s;however,thephenotypeofthesolitarytractnucleus(NTS)neuronsinvolvedisnotknown.A2/C2catecholamine(CA)neuronsintheNTSaredirectlyactivatedbyvisceralafferentsandareimportantforthecontroloffoodintakeandcardiovascularfunction,makingthemgoodcandidatestorespondtoandmediatetheeffectsofseroto
4、ninattheleveloftheNTS.Thisstudyexaminesserotonin’seffectsonNTS-CAneuronsusingpatch-clamptechniquesandtransgenicmiceexpress-inganenhancedgreenfluorescentproteindrivenbythetyrosinehydroxylase(TH)promoter(TH-EGFP)toidentifycatecholamineneurons.Serotoninincreasedthefrequencyofspontaneou
5、sglutamateexcitatorypostsynapticcurrents(sEPSCs)in90%ofNTS-TH-EGFPneurons,aneffectblockedbythe5-HT3receptorantagonistondansetronandmimickedbythe5-HT3receptoragonistsSR5227andmCPBG.Incontrast,5-HT3receptoragonistsincreasedsEPSCsonaminority(30%)ofnon-THneurons.5-HT3receptoragonistsi
6、ncreasedthefrequency,butnottheamplitude,ofmini-EPSCs,suggestingthattheiractionsarepresynaptic.5-HT3receptoragonistsincreasedthefiringrateofTH-EGFPneurons,aneffectdependentontheincreasedspontaneousglutamateinputsasitwasblockedbytheionotropicglutamateantagonistNBQX,butindependentofvis
7、ceralafferentactivation.TheseresultsdemonstrateacellularmechanismbywhichserotoninactivatesNTS-THneuronsandsuggestapathwaybywhichitcanincreasecatecholaminereleaseintargetregionstomodulatefoodintake,motivation,stress,andcardiovascularfunction.Introductionlateglutamaterelease(Glaumetal
8、.,1992;WanandBrowni
