Received1999204215Revised19992052243CorrespondencetoProf.HERui2Rong.Phn:862311260424121,ext15566;Fax:862311260428177;E2mail:syho@sjz1col1com1cnActaPhysiologicaSinica667Dec.1999,51(6),667～674EFFECTOFINTRACAROTIDADMINISTRATIONOFADENOSINEONTHEACTIVITYOFAREAPOSTREMANEURONSINBARODENERVATEDRATSCHENSHUANG,HERUI2RONG3(DepartmentofPhysiology,HebeiMedicalUniversity,Shijiazhuang050017)ABSTRACTToobservetheeffectofintracarotidadministrationofadenosineontheelectricalactivityofareapostrema(AP)neurons,76spontaneousactiveunitswererecordedfrom45sino2aorticdenervatedSprague2Dawleyratsusingextracellularrecordingtechnique.Theresultsobtainedareasfollows.(1)Follow2ingintracarotidadministrationofadenosine(Ado,25μg/kg),thedischargerateof29outof42unitsde2creasedmarkedlyfrom6126±0175to4174±0176spikes/s(P<0101),whereasthatof6unitsincreasedfrom4113±0177to4172±0183spikes/s(P<0105),andtheother7showednoresponse.Bloodpressure(BP)andheartrate(HR)wereunalteredthroughouttheexperiment.(2)82phenyltheophylline(82PT,15μg/kg),anonselectiveadenosinereceptorantagonist,completelyblockedtheinhibitoryeffectofAdoin10u2nits.(3)SelectiveA1adenosinereceptorantagonist,82cyclopentyl21,32dipropylxanthine(DPCPX,50μg/kg),blockedtheeffectofAdoin12unitstoaremarkableextent.(4)Glibenclamide(500μg/kg),ablockerofATP2sensitivepotassiumchannel,abolishedtheeffectofAdoin12units.TheaboveresultsindicatethatAdocaninhibitspontaneouselectricalactivityofAPneurons,whichismediatedbyadenosineA12receptorwiththeinvolvementofATP2sensitivepotassiumchannels.Keywords:adenosine;areapostrema;spontaneoussingle2unitdischarge;82phenyltheophylline;82cyclopentyl21,32dipropylxanthine;glibenclamideAdenosine(Ado)mayplayaroleasacentralmodulatorincardiovascularregulation[1].OurpreviousstudydemonstratedthatAdodoesresultinanenhancedneuronalexpressionofFos(amarkerofneuronalactivation)inbaroreflexpathway,includingthenucleusofthesolitarytract(NTS),areapostrema(AP)androstralventrolateralmedulla(RVLM)[2],specificallyintheAP.SucharesultsuggeststhatAdoisabletoaffecttheactivityofsomeregionsinCNSinvolvedinthebaroreflexfunc2tion,especiallyinAP.Furthermore,wehaveshowedthatAdoexertsaninhibitoryactiononthespon2taneouselectricalactivityofRVLMneurons[3],whichreceiveprojectionsfromAP[4].ItiswellknownthattheAPisacircumventricularorganlocatedonthedorsalsurfaceofthemedulla,andithasadensevascularsupplyandlackstheblood2brainbarrierandthusevenallowscirculatingpeptidestogaindirectaccesstospecificcentralneuralcomponentswithintheAP.Substantialevidencedocumented©1995-2005TsinghuaTongfangOpticalDiscCo.,Ltd.Allrightsreserved.thatAPisanimportantsiteinvolvedincardiovascularregulation[5].PreviousstudieshaveshownthatAPneuronsmightbeexcitedbycirculatingargininevasopressin(AVP)[6],endothelin[7,8]andan2giotensinII(ANGII)[9].InastudyofourlabastrongcasewasbuiltfortheAPasthesitewhereAVPactedtoaugmentthebaroreflex[10].SoitisproposedthatAPmayparticipateintheAdo2inducedfacilitationofbaroreflex.However,owingtothesuperficiallocationofAPonthemedullaoblongataandthesmallsizeoftheneurons,itisdifficulttokeeptheAPstableforlong2lastingelectro2physiologicalrecording.Uptonow,fewelectrophysiologicalstudieshaveattemptedtoelucidatethedi2recteffectofAdoontheelectricalactivityofAPneurons.ThepurposeofourstudywastoinvestigatetheeffectofAdoonthespontaneouselectricalactivityofAPneuronsandtoidentifytheinvolvedsub...
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