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Hotline:400-820-3792Inhibitors • ScreeningLibraries • Proteinswww.MedChemE5,7-DihydroxytryptaminehydrobromideCat.No.:HY-N18471ACASNo.:1841081-30-8Synonyms:5,7-DHPhydrobromide分子式:C₁₀H₁₃BrN₂O₂分子量:273.13作用靶点:5-HTReceptor;AdrenergicReceptor作用通路:GPCR/GProtein;NeuronalSignaling储存方式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY生物活性5,7-Dihydroxytryptamine(5,7-DHT)hydrobromide是一种神经毒素,选择性损伤大脑中的血清素能(5-HT)和去甲肾上腺素能(NE)神经元。5,7-Dihydroxytryptaminehydrobromide作为自体荧光的血清素衍生物,可与这些神经元的高亲和力转运体结合并被选择性摄取,随后在细胞内代谢产生活性氧自由基,导致轴突末梢退行性变和神经化学物质耗竭。5,7-Dihydroxytryptaminehydrobromide可用于神经科学研究[1][2][3][4]。体外研究5,7-Dihydroxytryptamine(25μM;60min)hydrobromidespecificallylabelsserotonergiccells(notTH-immunoreactivedopaminergiccells)inprimarymesencephalicculturesfrom14-day-oldWistarratfoetuses[3].5,7-Dihydroxytryptamine(20nM;15min)hydrobromidelesionsofascending5-HTpathwaysreduceinvitro3H-5-HTuptakeinratcortexcerebriandhypothalamussliceswithoutsignificantlyaltering3H-NAuptake[4].体内研究5,7-Dihydroxytryptamine(8μg;bilateralstereotaxicinfusionintonucleusaccumbens;2min)hydrobromideinducesahyperacusis-likebehaviorinWistarrats,asevidencedbysignificantlyincreasedacousticstartlereflexamplitudesintheabsenceofbackgroundnoise[1].5,7-Dihydroxytryptamine(12.5-50μg;i.c.v.)hydrobromideproducesdose-dependentdepletionsofhippocampalnorepinephrineandserotonininC57BL/6mice[2].5,7-Dihydroxytryptamine(4µgperinjectionsite;stereotacticinjection;1µL/minrate)hydrobromideproducesselectivechemicallesionsofascending5-HTpathwaysthatreduced3H-5-HTuptakeincorticalandhypothalamicterminalareas(withoutsignificanteffectson3H-NAuptake),inducedmousekillingbehavior,increasedshock-elicitedboxingpositions,reducedhabituationratetosensorystimuli,anddidnotsignificantlyalterhomecageactivity[4].1/3 MasterofBioactiveMolecules—您身边的抑制剂大师www.MedChemEAnimalModel:Wistarrats(adultmale,175-200gatsurgery)[1]Dosage:8μgAdministration:bilateralstereotaxicinfusionintonucleusaccumbens;over2min,injectorleftinplacefor1additionalminpost-infusionResult:IncreasedmeanamplitudeoftheacousticstartlereflexsignificantlyacrossallstimulusintensitiesintheabsenceofbackgroundnoisecomparedtotheSham-lesiongroup.ShowednosignificantdifferencesinstartleamplitudebetweentheDHT-lesion,Sham-lesion,andintactgroupsatanystimulusintensityinthepresenceofbackgroundnoise.Confirmednearlycompletelossofserotonergicneuronsinthenucleusaccumbensviaimmunohistochemistry.AnimalModel:C57BL/6(male,2and10monthsold,20-30g)[2]Dosage:12.5μg;25μg;50μgAdministration:i.c.v.;singledoseResult:Hadadamagingeffectonthenoradrenergicsystem,andthiseffectwasindependentoftheageofthemice.Exertedstrongertoxiceffectsonserotonergicneuronsinyoungindividuals.AnimalModel:M/511-Wistar(male,240-280g)[4]Dosage:4µg(calculatedasthebase)perinjectionsiteAdministration:stereotacticinjection;1µl/minrate;needleleftinsitufor1minpost-injectionResult:Reduced³H-5-HTuptakebutdidnotchange³H-NAuptakeinthecortex(medialbundlelesiongroup).Reduced³H-NAuptaketo75%ofcontrol(non-significant)inthecortex(medialpluslateralbundlelesiongroup).Inducedmousekillingbehaviorin4of8rats(medialbundlelesiongroup)and6of7rats(medialpluslateralbundlelesiongroup).Requiredsignificantlymoretrialstoreachhabituationcriterionfortouch(bothlesiongroups).Requiredsignificantlymoretrialsforacousticstimulationhabituation(onlymedialpluslaterallesiongroup).Showedasignificantlyhighernumberofboxingpositionsintheshockelicitedfightingtest(bothlesiongroups).Showednosignificantchangesinhomecageactivity(bothlesiongroups).REFERENCES2/3 MasterofBioactiveMolecules—您身边的抑制剂大师www.MedChemEFarahaniS,etal.Does5,7-Dihydroxytryptamineinjectionintonucleusaccumbenscausehyperacusis?.NeurosciLett.2019;705:246-250.FinneganKT,etal.Theamine-depletingeffectsof5,7-dihydroxytryptamine(5,7-DHT)inC57BL/6micedonotincreasewithage.BrainRes.1989;496(1-2):251-256.FrankeH,etal.5,7-Dihydroxytryptamine--aselectivemarkerofdopaminergicorserotonergicneurons?.NaunynSchmiedebergsArchPharmacol.2002;366(4):315-318.HoleK,etal.5,7-Dihydroxytryptaminelesionsoftheascending5-hydroxytryptaminepathways:habituation,motoractivityandagonisticbehavior.PharmacolBiochemBe

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