2021
Dopamine D1R Receptor Stimulation as a Mechanistic Pro-cognitive Target for Schizophrenia
Abi-Dargham A, Javitch JA, Slifstein M, Anticevic A, Calkins ME, Cho YT, Fonteneau C, Gil R, Girgis R, Gur RE, Gur RC, Grinband J, Kantrowitz J, Kohler C, Krystal J, Murray J, Ranganathan M, Santamauro N, Van Snellenberg J, Tamayo Z, Wolf D, D’Souza D, Srihari V, Gueorguieva R, Patel P, Forselius-Bielen K, Lu J, Butler A, Fram G, Afriyie-Agyemang Y, Selloni A, Cadavid L, Gomez-Luna S, Gupta A, Radhakrishnan R, Rashid A, Aker R, Abrahim P, Nia A, Surti T, Kegeles L, Carlson M, Goldberg T, Gangwisch J, Benedict E, Govil P, Brazis S, Mayer M, de la Garrigue N, Fallon N, Baumvoll T, Abeykoon S, Perlman G, Bobchin K, Elliott M, Schmidt L, Rush S, Port A, Heffernan Z, Laney N, Kantor J, Hohing T, Gray D, Lieberman J. Dopamine D1R Receptor Stimulation as a Mechanistic Pro-cognitive Target for Schizophrenia. Schizophrenia Bulletin 2021, 48: 199-210. PMID: 34423843, PMCID: PMC8781338, DOI: 10.1093/schbul/sbab095.Peer-Reviewed Original ResearchConceptsCortical dopamine neurotransmissionPositive allosteric modulationImportant therapeutic targetPF-06412562Dopaminergic receptorsD1R stimulationDA levelsTolerable dosesLevel of stimulationDopamine neurotransmissionReceptor stimulationTherapeutic targetPartial agonistCognitive deficitsBiased agonismFull agonismTarget engagementAllosteric modulationNew drugsStimulationPoor bioavailabilitySchizophreniaOptimal stimulationDrugsExpression levels
2017
Systemic inflammation enhances stimulant-induced striatal dopamine elevation
Petrulli J, Kalish B, Nabulsi N, Huang Y, Hannestad J, Morris E. Systemic inflammation enhances stimulant-induced striatal dopamine elevation. Translational Psychiatry 2017, 7: e1076-e1076. PMID: 28350401, PMCID: PMC5404612, DOI: 10.1038/tp.2017.18.Peer-Reviewed Original ResearchMeSH KeywordsAdultCarbon RadioisotopesCase-Control StudiesCentral Nervous System StimulantsDopamineDopamine AntagonistsFemaleHealthy VolunteersHumansInflammationInterleukin-6Interleukin-8LipopolysaccharidesMaleMethylphenidateNeostriatumPositron-Emission TomographyRacloprideRadiopharmaceuticalsReceptors, Dopamine D2Tumor Necrosis Factor-alphaYoung AdultConceptsDA elevationSystemic inflammationImmune activationTumor necrosis factor alphaAcute immune activationImmune activator lipopolysaccharideOral methylphenidate (MPH) challengeStriatal DA levelsIL-8 concentrationsNecrosis factor alphaMesolimbic dopamine systemCross-over designPositron emission tomographyNeuroimmune systemMethylphenidate challengeDA levelsDA transmissionDopamine elevationDA dysfunctionFactor alphaBaseline scanHealthy subjectsAntagonist tracersPlaceboDopamine system
2014
Histidine Decarboxylase Deficiency Causes Tourette Syndrome: Parallel Findings in Humans and Mice
Baldan LC, Williams KA, Gallezot JD, Pogorelov V, Rapanelli M, Crowley M, Anderson GM, Loring E, Gorczyca R, Billingslea E, Wasylink S, Panza KE, Ercan-Sencicek AG, Krusong K, Leventhal BL, Ohtsu H, Bloch MH, Hughes ZA, Krystal JH, Mayes L, de Araujo I, Ding YS, State MW, Pittenger C. Histidine Decarboxylase Deficiency Causes Tourette Syndrome: Parallel Findings in Humans and Mice. Neuron 2014, 81: 77-90. PMID: 24411733, PMCID: PMC3894588, DOI: 10.1016/j.neuron.2013.10.052.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAmphetamineAnimalsBrainChildDopamine AgonistsDopamine AntagonistsExploratory BehaviorFemaleHistidine DecarboxylaseHumansMaleMaze LearningMiceMice, KnockoutMiddle AgedMutationOxazinesRacloprideRadionuclide ImagingStereotyped BehaviorTime FactorsTourette SyndromeTryptophanYoung AdultConceptsTourette syndromeHA infusionKnockout miceD2/D3 receptor bindingDecarboxylase deficiencyDopamine D2 antagonist haloperidolCortico-basal ganglia circuitsStriatal DA levelsHDC knockout miceD3 receptor bindingImmediate early gene FosD2 antagonist haloperidolRare genetic causeBiosynthesis of histamineStriatal DARare causeBasal gangliaDA levelsAntagonist haloperidolGanglia circuitsPrepulse inhibitionMiceReceptor bindingGenetic causeHistidine decarboxylase
2007
Behavioral improvement in a primate Parkinson's model is associated with multiple homeostatic effects of human neural stem cells
Redmond DE, Bjugstad KB, Teng YD, Ourednik V, Ourednik J, Wakeman DR, Parsons XH, Gonzalez R, Blanchard BC, Kim SU, Gu Z, Lipton SA, Markakis EA, Roth RH, Elsworth JD, Sladek JR, Sidman RL, Snyder EY. Behavioral improvement in a primate Parkinson's model is associated with multiple homeostatic effects of human neural stem cells. Proceedings Of The National Academy Of Sciences Of The United States Of America 2007, 104: 12175-12180. PMID: 17586681, PMCID: PMC1896134, DOI: 10.1073/pnas.0704091104.Peer-Reviewed Original ResearchConceptsHuman neural stem cellsSubstantia nigraParkinson's diseaseNeural stem cellsTyrosine hydroxylaseBehavioral improvementModel of PDHost substantia nigraStem cellsResponsive progenitor cellsAlpha-synuclein aggregationDA markersNigrostriatal circuitryParkinsonian primatesParkinsonian signsNeuronal numberDA levelsFunctional improvementParkinson modelImmunopositive cellsNormalizing effectDA phenotypeHomeostatic effectsNumber of diseasesProgenitor cells
2006
Differential effects of nicotinic antagonists perfused into the nucleus accumbens or the ventral tegmental area on cocaine-induced dopamine release in the nucleus accumbens of mice
Zanetti L, Picciotto MR, Zoli M. Differential effects of nicotinic antagonists perfused into the nucleus accumbens or the ventral tegmental area on cocaine-induced dopamine release in the nucleus accumbens of mice. Psychopharmacology 2006, 190: 189. PMID: 17061109, DOI: 10.1007/s00213-006-0598-6.Peer-Reviewed Original ResearchConceptsIntra-VTA perfusionVentral tegmental areaDA levelsNucleus accumbensCocaine-elicited increasesPerfusate levelsTegmental areaCocaine-induced dopamine releaseNicotinic acetylcholine receptor antagonistMesolimbic DA neuronsDihydro-β-erythroidineAcetylcholine receptor antagonistEffects of cocaineMesolimbic dopamine systemSubtype-specific mannerDA neuronsNAChR antagonistIntracerebral microdialysisNicotinic antagonistsReceptor antagonistNicotinic pathwayLocal perfusionDopamine releaseDopamine systemPerfusionInhibition of both α7* and β2* nicotinic acetylcholine receptors is necessary to prevent development of sensitization to cocaine-elicited increases in extracellular dopamine levels in the ventral striatum
Zanetti L, de Kerchove D’Exaerde A, Zanardi A, Changeux JP, Picciotto MR, Zoli M. Inhibition of both α7* and β2* nicotinic acetylcholine receptors is necessary to prevent development of sensitization to cocaine-elicited increases in extracellular dopamine levels in the ventral striatum. Psychopharmacology 2006, 187: 181-188. PMID: 16826402, DOI: 10.1007/s00213-006-0419-y.Peer-Reviewed Original ResearchConceptsExtracellular dopamine levelsDevelopment of sensitizationWild-type miceDopamine levelsVentral striatumCocaine-elicited increasesExtracellular DA levelsAdministration of cocaineDihydro-β-erythroidineAbility of cocaineNicotinic acetylcholine receptorsNicotine treatmentDA levelsNicotinic antagonistsRationaleSeveral studiesNeurochemical responsesConclusionsThese dataObjectivesThe current studySpecific antagonistNAChR blockadeAcetylcholine receptorsElicit increasesStriatumMiceSensitization
2002
Acute and long‐term changes in the mesolimbic dopamine pathway after systemic or local single nicotine injections
Ferrari R, Le Novère N, Picciotto MR, Changeux JP, Zoli M. Acute and long‐term changes in the mesolimbic dopamine pathway after systemic or local single nicotine injections. European Journal Of Neuroscience 2002, 15: 1810-1818. PMID: 12081661, DOI: 10.1046/j.1460-9568.2001.02009.x.Peer-Reviewed Original ResearchMeSH KeywordsAmphetamineAnimalsDopamineDopamine Plasma Membrane Transport ProteinsDrug Administration RoutesExtracellular SpaceHabituation, PsychophysiologicMaleMembrane GlycoproteinsMembrane Transport ProteinsMicrodialysisMotor ActivityNerve Tissue ProteinsNeural PathwaysNeuronal PlasticityNicotineNucleus AccumbensPresynaptic TerminalsRatsRats, Sprague-DawleyReceptors, AMPAReceptors, N-Methyl-D-AspartateRNA, MessengerSubstance-Related DisordersTime FactorsTyrosine 3-MonooxygenaseVentral Tegmental AreaConceptsDialysate DA levelsGluR1 mRNA levelsSingle nicotine injectionNicotine administrationDA levelsMesolimbic dopamine pathwayNicotine injectionTyrosine hydroxylaseDopamine pathwayMRNA levelsBasal DA levelsExtracellular DA levelsMesolimbic DA pathwaySystemic intraperitoneal injectionTH mRNA levelsIntra-accumbens infusion
2001
Embryonic ventral mesencephalic grafts to the substantia nigra of MPTP‐treated monkeys: Feasibility relevant to multiple‐target grafting as a therapy for Parkinson's disease
Collier TJ, Sortwell CE, Elsworth JD, Taylor JR, Roth RH, Sladek JR, Redmond DE. Embryonic ventral mesencephalic grafts to the substantia nigra of MPTP‐treated monkeys: Feasibility relevant to multiple‐target grafting as a therapy for Parkinson's disease. The Journal Of Comparative Neurology 2001, 442: 320-330. PMID: 11793337, DOI: 10.1002/cne.10108.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsBrain Tissue TransplantationCell DifferentiationChlorocebus aethiopsDopamineGraft SurvivalHomovanillic AcidImmunohistochemistryMaleNeostriatumNerve RegenerationNeuritesNeuronsParkinsonian DisordersRecovery of FunctionStem Cell TransplantationStem CellsSubstantia NigraTreatment OutcomeTyrosine 3-MonooxygenaseConceptsSubstantia nigraParkinson's diseaseDA neuronsVentral mesencephalonTyrosine hydroxylaseTH-positive fiber densityEmbryonic DA neuronsEmbryonic dopamine neuronsRostral substantia nigraStriatal DA depletionVentral mesencephalic graftsBasal ganglia circuitryBasal ganglia structuresSuboptimal therapeutic outcomesAfrican green monkeysDA modulationGrafted neuronsVM graftsMesencephalic graftsParkinsonian monkeysSN neuronsDA depletionReplacement therapyDA replacementDA levels
1998
Depletion of dopamine in the nucleus accumbens prevents the generation of locomotion by metabotropic glutamate receptor activation
Meeker D, Kim J, Vezina P. Depletion of dopamine in the nucleus accumbens prevents the generation of locomotion by metabotropic glutamate receptor activation. Brain Research 1998, 812: 260-264. PMID: 9813358, DOI: 10.1016/s0006-8993(98)00941-x.Peer-Reviewed Original ResearchConceptsMetabotropic glutamate receptor activationDepletion of dopamineMetabotropic glutamate receptorsGlutamate receptor activationMicroinjection of salineGroups of ratsNon-lesioned animalsContribution of dopamineMGluR agonistBilateral microinjectionDA levelsMGluR activationDA neurotransmissionGlutamate receptorsNucleus accumbensMicroinjection sitesLocomotor activityReceptor activationRatsEnhanced locomotionDopamineGeneration of locomotionAMPHNAccSaline
1990
3-Acetylpyridine results in degeneration of the extrapyramidal and cerebellar motor systems: loss of the dorsolateral striatal dopamine innervation
Deutsch A, Elsworth J, Roth R, Menek G. 3-Acetylpyridine results in degeneration of the extrapyramidal and cerebellar motor systems: loss of the dorsolateral striatal dopamine innervation. Brain Research 1990, 527: 96-102. PMID: 2126479, DOI: 10.1016/0006-8993(90)91065-o.Peer-Reviewed Original ResearchConceptsCerebellar motor systemsDopamine innervationOlivocerebellar systemStriatal DA depletionStriatal dopamine innervationStriatal DA concentrationsMotor systemSelective inhibitor deprenylAnteromedial prefrontal cortexDeprenyl pretreatmentStriatal sectorsNigrostriatal degenerationDA innervationDA depletionDA levelsVentromedial striatumMAOB activitySensorimotor functionRats resultsNucleus accumbensDorsolateral aspectDorsolateral striatumMAOA activityDegenerationPrefrontal cortexMesocortical dopamine neurons: High basal firing frequency predicts tyrosine dependence of dopamine synthesis
Tam S, Elsworth J, Bradberry C, Roth R. Mesocortical dopamine neurons: High basal firing frequency predicts tyrosine dependence of dopamine synthesis. Journal Of Neural Transmission 1990, 81: 97-110. PMID: 2363911, DOI: 10.1007/bf01245830.Peer-Reviewed Original ResearchConceptsMesoprefrontal DA neuronsDA neuronsTyrosine administrationDA levelsCingulate cortexPrefrontal cortexTyrosine hydroxylationAnxiogenic β-carbolineDA metabolite levelsDA terminal fieldsEndogenous DA levelsMesocortical DA neuronsMesocortical dopamine neuronsVivo tyrosine hydroxylationMidbrain DA neuronsTyrosine hydroxylase activityTransmitter outflowDA metabolitesDA synthesisDopamine neuronsFG 7142Dopamine synthesisTerminal fieldsTyrosine availabilityHigh doses
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