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Involvement

By Doris Russell,2014-02-18 10:49
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Involvement

    Involvement

    二十三

    InvolvementofcAMP/cAMP--dependentproteihakinase

    signalingpathwayinregulationofNa,KATPaseupon

    activationofopioidreceptorsbymorphine

    LiuJingGenWuZha0Qiu

    StateKeyLaboratoryofDrugResearch,ShanghaiInstituteofMateriaMedics,Shanghai201203

    ThedepolarizationofneuronsinducedbyimpairmentofNa.K

    ATPase.activityafterchronico

    platetreatmenthasbeenshowntoinvolvethedevelopmentofopioiddependence.However,themecha-

    nismsunderlyingchangesinNa,K

    ATPaseactivityfollowingopioidtreatmentareunclear.Thebest

    establishedmolecularadaptationtochronicopioidexposureisup..regulationofthecAMP/PKAsigna

    lingpathway,thisstudy,therefore,wasundertakentoinvestigatetheroleofup

    regulationofcAMP/

    PKAsignalingpathwayinalterationofthemousehippocampalNa,K

    ATPaseactivity.Theresults

    demonstratedthatacutemorphinetreatmentdosedependentlystimulatedNa,K

    ATPaseactivity.

    Thi8actioncouldbesignificantlysuppressedbyadenylylcyclaseactivatorforskolin,orthecAMPana

    loguedb

    cAMP.Contrarytoacutemorphinetreatment,chronicmorphinetreatmentsignificantlyinhibi

tedNa.KATPaseactivity.Moreover,anadditionaldecreaseinNa,K

    ATPaseactivitywas

    observedbvnaloxoneprecipitation.TheeffectsofbothacuteandchronicmorphinetreatmentonNa,

    KATPaseactivitvwerenaltrexonereversible.TheregulationofNa,K

    ATPaseactivityby

    morphinewasinverselvcclrrelatedwithintracellularcAMPaccumulation.H

    89,aspecificPKAinhibi

    tor.mimickedthestimulatoryeffectofacutemorphinebutantagonizedtheinhibitoryeffectofchronic

    morDhineonNa.K

    ATPaseactivity.However,okadaicacid,aproteinphosphataseinhibitor,sup

    DressedacutemorphinestimulationbutpotentiatedchronicmorphineinhibitionofNa,K

    ATPase

    theaherationinphosphorylationlevel,butnottoberelevanttothechangeinabundanceofNa,K

    ATPase.ThesefindingsstronglydemonstratethatcAMP/PKAsignalingpathwayinvolvesinregulationof

    Na.KATPaseactivityafteractivationofopioidreceptors.

    InfluenceofcalciumchannelblockersonGABAAreceptor

    ZhangYongHe(张永鹤)

    DepartmentofPharmacology,Schoolof

    ZhaoXinCuiXiang--Yu

    BasicMedicalScience,PekingUniversity

    Thisstudywasundertakentoaddresseffectsoftheinteractionsbetweencalciumtransientsandserotonerglcact,onon

    theregulati0nofs1eeparchitectureandcF0

    expression(asamarkerofneuronalactivation)inVLPOandTMNinduced

    bypentobarbital(PB)andtheinfluenceofCa?channelblockers(CCB)onGABA^receptor.

    Theresultsshowedthatbisbenzylisoquinolinealkaloidtetrandrine,dihydropyridinederivat

ivenifedipineandother

    type8ofCCB.verapamilanddiltiazem(DT)increasedboththesleepingtimeinhypnoticdosageofPB(45mg/kg.ip)

    treatedmiceandtherateofsleeponsetinthesubhypnoticdosageofPB(28mg/kg,ip)treatedmiceinadosedependent

    manner,respectively,andtheseeffectsweresignificantlyaugmentedby5

    HTP,theimmediateprecursorof5HTand

    antagonizedbypretreatmentofP

    chlorophenylalanine(PCPA),aninhibitoroftryptophanhydroxylase.DT,themostpo 12

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