Direct Effects of HIV-1 Tat on Excitability and Survival of Primary Dorsal Root Ganglion Neurons Possible Contribution to HIV-1-Associated Pain 英文参考文献.docVIP

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Direct Effects of HIV-1 Tat on Excitability and Survival of Primary Dorsal Root Ganglion Neurons Possible Contribution to HIV-1-Associated Pain 英文参考文献.doc

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Direct Effects of HIV-1 Tat on Excitability and Survival of Primary Dorsal Root Ganglion Neurons Possible Contribution to HIV-1-Associated Pain 英文参考文献

DirectEffectsofHIV-1TatonExcitabilityandSurvivalof PrimaryDorsalRootGanglionNeurons:Possible ContributiontoHIV-1-AssociatedPain XianxunChi1.,TohtiAmet2.,DanielByrd2,Kuei-HuaChang3,KavitaShah3,NingjieHu2 ,Ayslinn Grantham2,SishunHu2,JianhongDuan1,FengTao4,GrantNicol1,QiguiYu2* 1DepartmentofPharmacologyandToxicology,IndianaUniversitySchoolofMedicine,Indianapolis,Indiana,UnitedStatesofAmerica,2CenterforAIDSResearchand DepartmentofMicrobiologyandImmunology,IndianaUniversitySchoolofMedicine,Indianapolis,Indiana,UnitedStatesofAmerica, 3DepartmentofChemistryand PurdueUniversityCenterforCancerResearch,PurdueUniversity,WestLafayette,Indiana,UnitedStatesofAmerica, 4DepartmentofAnesthesiologyandCriticalCare Medicine,JohnsHopkinsUniversitySchoolofMedicine,Baltimore,Maryland,UnitedStatesofAmerica Abstract The vast majority of people living with human immunodeficiency virus type 1 (HIV-1) have pain syndrome, which has a significantimpactontheirqualityoflife.TheunderlyingcausesofHIV-1-associatedpainarenotlikelyattributabletodirect viralinfectionofthenervoussystemduetothelackofevidenceofneuronalinfectionbyHIV-1.However,HIV-1proteinsare possiblyinvolvedastheyhavebeenimplicatedinneuronaldamageanddeath.Thecurrentstudyassessesthedirecteffects ofHIV-1Tat,oneofpotentneurotoxicviralproteinsreleasedfromHIV-1-infectedcells,ontheexcitabilityandsurvivalofrat primarydorsalrootganglion(DRG)neurons.WedemonstratedthatHIV-1Tattriggeredrapidandsustainedenhancement of the excitability of small-diameter rat primary DRG neurons, which was accompanied by marked reductions in the rheobaseandrestingmembranepotential(RMP),andanincreaseintheresistanceatthreshold(RTh).SuchTat-inducedDRG hyperexcitabilitymaybeaconsequenceoftheinhibitionofcyclin-dependentkinase5(Cdk5)activity.Tatrapidlyinhibited Cdk5kinaseactivityandmRNAproduction,androscovitine,awell-knownCdk5inhibitor,inducedaverysimilarpatternof DRGhyperexcitability.Indeed,pre-applicationofTatpreventedroscovitinefromhavingadditionaleffect