2009
Prior chronic cocaine exposure in mice induces persistent alterations in cognitive function
Krueger DD, Howell JL, Oo H, Olausson P, Taylor JR, Nairn AC. Prior chronic cocaine exposure in mice induces persistent alterations in cognitive function. Behavioural Pharmacology 2009, 20: 695-704. PMID: 19901826, PMCID: PMC3380449, DOI: 10.1097/fbp.0b013e328333a2bb.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAttentionCocaineCocaine-Related DisordersCognitionConditioning, ClassicalConditioning, OperantDisease Models, AnimalImpulsive BehaviorInhibition, PsychologicalInjections, IntraperitonealMaleMemory DisordersMemory, Short-TermMiceMice, Inbred C57BLMotor ActivityReinforcement ScheduleReinforcement, PsychologyReversal LearningTime FactorsConceptsCognitive functionAttentional functionsResponse inhibitionPrefrontal cortexThree-choice serial reaction time taskSerial reaction time taskReaction time taskPattern of errorsCocaine exposureDevelopment of addictionPrior chronic exposureCognitive flexibilityInstrumental reversalTime taskPosition taskChronic cocaine exposureChronic cocaine useCognitive dysfunctionTaskMemoryCocaine useDrug-free periodSuitable animal modelMultiple aspectsCortex
1999
Striatal dopaminergic correlates of stable parkinsonism and degree of recovery in old-world primates one year after MPTP treatment
Elsworth J, Taylor J, Sladek J, Collier T, Redmond D, Roth R. Striatal dopaminergic correlates of stable parkinsonism and degree of recovery in old-world primates one year after MPTP treatment. Neuroscience 1999, 95: 399-408. PMID: 10658619, DOI: 10.1016/s0306-4522(99)00437-6.Peer-Reviewed Original ResearchConceptsHomovanillic acid/dopamine ratioMPTP treatmentStriatal dopamine levelsDopamine levelsDopamine lossDopamine depletionDopamine ratioStriatal subregionsNucleus accumbensCaudate nucleusDopamine concentrationsOne-yearSeverity categoriesDopamine neuron integrityVentromedial caudate nucleusStriatal dopamine lossHomovanillic acid concentrationsStriatal dopaminergic functionMarked increaseNormal motor performancePaucity of dataMetabolic activityNon-human primatesParkinsonian disabilityTetrahydropyridine (MPTP) modelEnhancement of Locomotor Activity and Conditioned Reward to Cocaine by Brain-Derived Neurotrophic Factor
Horger B, Iyasere C, Berhow M, Messer C, Nestler E, Taylor J. Enhancement of Locomotor Activity and Conditioned Reward to Cocaine by Brain-Derived Neurotrophic Factor. Journal Of Neuroscience 1999, 19: 4110-4122. PMID: 10234039, PMCID: PMC6782687, DOI: 10.1523/jneurosci.19-10-04110.1999.Peer-Reviewed Original ResearchConceptsBrain-derived neurotrophic factorDevelopment of sensitizationLocomotor sensitizationBDNF infusionNeurotrophic factorNucleus accumbensStimulant effectsInitial stimulant effectMesolimbic DA systemCocaine-induced locomotionVentral tegmental areaMesolimbic dopamine systemWild-type littermatesPsychomotor stimulant effectsBDNF administrationDopaminergic neuronsTegmental areaCocaine injectionCocaine dosesControl animalsDopamine systemLocomotor activityDrug rewardCR leverDA systemEnhanced responding for conditioned reward produced by intra-accumbens amphetamine is potentiated after cocaine sensitization
Taylor J, Horger B. Enhanced responding for conditioned reward produced by intra-accumbens amphetamine is potentiated after cocaine sensitization. Psychopharmacology 1999, 142: 31-40. PMID: 10102780, DOI: 10.1007/s002130050859.Peer-Reviewed Original ResearchConceptsIntra-accumbens amphetamineIntra-NAc amphetamineCocaine sensitizationLocomotor sensitizationNucleus accumbensCR leverLong-term neuronal adaptationsSaline-treated groupMesolimbic dopamine systemStimulant drug useSaline infusionSaline injectionDopamine systemPsychomotor stimulantsDrug useNeuronal adaptationConditioned rewardStimulant drugsAmphetaminePrior exposureSensitizationTest daySeparate groupsNCR leverPredictive associations
1998
Subchronic Phencyclidine Administration Increases Mesolimbic Dopaminergic System Responsivity and Augments Stress- and Psychostimulant-Induced Hyperlocomotion
Jentsch J, Taylor J, Roth R. Subchronic Phencyclidine Administration Increases Mesolimbic Dopaminergic System Responsivity and Augments Stress- and Psychostimulant-Induced Hyperlocomotion. Neuropsychopharmacology 1998, 19: 105-113. PMID: 9629564, DOI: 10.1016/s0893-133x(98)00004-9.Peer-Reviewed Original ResearchMeSH Keywords3,4-Dihydroxyphenylacetic AcidAnalysis of VarianceAnimalsBrainDextroamphetamineDisease Models, AnimalDizocilpine MaleateDopamineDrug Administration ScheduleHaloperidolLimbic SystemMaleMotor ActivityPhencyclidinePrefrontal CortexRatsRats, Sprague-DawleySchizophreniaStress, PsychologicalTime FactorsConceptsDopamine utilizationHaloperidol-induced increasePCP exposureFrontal cortical dysfunctionAmphetamine-induced hyperlocomotionSubchronic PCP administrationMesolimbic dopamine transmissionPCP-treated ratsCortical dopaminergicCortical dysfunctionDopaminergic deficitDopaminergic transmissionDopaminergic functionDopamine transmissionDopaminergic hypoactivityPCP administrationBehavioral pathologyCognitive deficitsRatsSystem responsivityHyperlocomotionDopaminergicExposureCurrent studyDeficitsPrefrontal cortical involvement in phencyclidine-induced activation of the mesolimbic dopamine system: behavioral and neurochemical evidence
Jentsch J, Tran A, Taylor J, Roth R. Prefrontal cortical involvement in phencyclidine-induced activation of the mesolimbic dopamine system: behavioral and neurochemical evidence. Psychopharmacology 1998, 138: 89-95. PMID: 9694531, DOI: 10.1007/s002130050649.Peer-Reviewed Original ResearchConceptsMesolimbic dopamine systemPrefrontal cortexInduced hyperlocomotionDopamine neuronsDopamine releaseNucleus accumbensDopamine systemInjection of phencyclidineMesocorticolimbic dopaminergic neuronsMesolimbic dopamine neuronsVentral tegmental areaCell body regionIbotenic acid lesionsPrefrontal Cortical InvolvementProfound cognitive impairmentGlutamatergic releaseNeurochemical evidenceAcute administrationCortical involvementDopamine utilizationDopaminergic neuronsMesolimbic pathwayTegmental areaAcid lesionsDopaminergic activation
1997
Opposite Modulation of Opiate Withdrawal Behaviors on Microinfusion of a Protein Kinase A Inhibitor Versus Activator into the Locus Coeruleus or Periaqueductal Gray
Punch L, Self D, Nestler E, Taylor J. Opposite Modulation of Opiate Withdrawal Behaviors on Microinfusion of a Protein Kinase A Inhibitor Versus Activator into the Locus Coeruleus or Periaqueductal Gray. Journal Of Neuroscience 1997, 17: 8520-8527. PMID: 9334424, PMCID: PMC6573752, DOI: 10.1523/jneurosci.17-21-08520.1997.Peer-Reviewed Original ResearchAmygdalaAnimalsBehavior, AnimalCyclic AMPCyclic AMP-Dependent Protein KinasesEnzyme InhibitorsInfusions, ParenteralLocus CoeruleusMaleMorphine DependenceMotor ActivityNaloxoneNarcotic AntagonistsNerve Tissue ProteinsPeriaqueductal GrayPhosphorylationProtein Processing, Post-TranslationalRatsRats, Sprague-DawleySecond Messenger SystemsStereotyped BehaviorSubstance Withdrawal SyndromeThionucleotidesTyrosine 3-Monooxygenase(S)-(-)-HA-966, a gamma-hydroxybutyrate-like agent, prevents enhanced mesocorticolimbic dopamine metabolism and behavioral correlates of restraint stress, conditioned fear and cocaine sensitization.
Morrow B, Lee E, Taylor J, Elsworth J, Nye H, Roth R. (S)-(-)-HA-966, a gamma-hydroxybutyrate-like agent, prevents enhanced mesocorticolimbic dopamine metabolism and behavioral correlates of restraint stress, conditioned fear and cocaine sensitization. Journal Of Pharmacology And Experimental Therapeutics 1997, 283: 712-21. PMID: 9353390.Peer-Reviewed Original ResearchConceptsHA-966Dopamine metabolismMedial prefrontal cortexCocaine sensitizationNucleus accumbensHigh doseAcute cocaine-induced locomotionPrefrontal cortexGABAB receptor bindingCocaine-induced locomotionGamma-aminobutyric acidStress-induced increaseFear-inducing behaviorDopamine utilizationGABAB receptorsRestraint stressControl ratsLocomotor sensitizationDopaminergic neurotransmissionShell subdivisionBaclofen bindingCortical membranesPositive enantiomerWeight gainReceptor binding
1995
R-(+)-HA-966, an antagonist for the glycine/NMDA receptor, prevents locomotor sensitization to repeated cocaine exposures
Morrow B, Taylor J, Roth R. R-(+)-HA-966, an antagonist for the glycine/NMDA receptor, prevents locomotor sensitization to repeated cocaine exposures. Brain Research 1995, 673: 165-169. PMID: 7757472, DOI: 10.1016/0006-8993(94)01456-r.Peer-Reviewed Original ResearchConceptsGlycine/NMDA receptorHA-966Locomotor sensitizationLocomotor activationNMDA receptorsCocaine administrationSubsequent challenge doseLocomotor stimulant propertiesNMDA receptor complexAcute stimulant effectsChallenge doseReverse toleranceRepeated administrationAcute doseCocaine exposureStimulant effectsGlycine receptorsStimulant propertiesCocaineSensitizationAdministrationReceptorsReceptor complexAntagonistDose
1994
Preexposure to, but Not Cotreatment with, the Neurotensin Antagonist SR 48692 Delays the Development of Cocaine Sensitization
Horger B, Taylor J, Elsworth J, Roth R. Preexposure to, but Not Cotreatment with, the Neurotensin Antagonist SR 48692 Delays the Development of Cocaine Sensitization. Neuropsychopharmacology 1994, 11: 215-222. PMID: 7865101, DOI: 10.1038/sj.npp.1380108.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCocaineMaleMotor ActivityPyrazolesQuinolinesRatsRats, Sprague-DawleyReceptors, NeurotensinTime FactorsConceptsCocaine challenge injectionSR 48692Role of neurotensinDevelopment of sensitizationEffects of cocaineCocaine sensitizationChallenge injectionDay drug-free periodMale Sprague-Dawley ratsCocaine-induced locomotor activityDrug-free periodSprague-Dawley ratsCocaine-induced locomotor activationCocaine-induced activityDrug-free daysEffects of cotreatmentPreexposure injectionsDaily administrationLocomotor activationCocaine testLocomotor deficitsLocomotor activityActivity countsChronic preexposureCocaine testing
1991
Grafting of fetal substantia nigra to striatum reverses behavioral deficits induced by MPTP in primates: a comparison with other types of grafts as controls
Taylor J, Elsworth J, Roth R, Sladek J, Collier T, Redmond D. Grafting of fetal substantia nigra to striatum reverses behavioral deficits induced by MPTP in primates: a comparison with other types of grafts as controls. Experimental Brain Research 1991, 85: 335-348. PMID: 1893983, DOI: 10.1007/bf00229411.Peer-Reviewed Original ResearchConceptsCaudate nucleusBehavioral deficitsHealthy behaviorsFetal substantia nigra cellsFetal substantia nigraIdiopathic Parkinson's diseasePoverty of movementType of graftDays/weekSubstantia nigra cellsTime of sacrificePre-treatment levelsSN cellsSpecific behavioral effectsMPTP treatmentMPTP toxicityParkinsonian signsSubstantia nigraControl subjectsInitiation of movementBrain sitesLimb tremorParkinson's diseaseControl animalsMPTPCocaethylene: A neuropharmacologically active metabolite assciated with concurrent cocaine-ethanol ingestion
Jatlow P, Elsworth JD, Bradberry CW, Winger G, Taylor JR, Russell R, Roth RH. Cocaethylene: A neuropharmacologically active metabolite assciated with concurrent cocaine-ethanol ingestion. Life Sciences 1991, 48: 1787-1794. PMID: 2020260, DOI: 10.1016/0024-3205(91)90217-y.Peer-Reviewed Original ResearchConceptsDopamine uptake systemEffects of cocaineExtracellular dopamine concentrationBlood of individualsSelf-administration studiesInhibition of bindingEthanol abuseSystemic administrationNucleus accumbensDopamine reuptakeLocomotor activityActive metaboliteDopamine concentrationsBehavioral effectsCocaineEffects of ECRatsVivo formationEquipotentInhibitionSame extent
1990
Cocaethylene inhibits uptake of dopamine and can reach high plasma concentrations following combined cocaine and ethanol use.
Jatlow P, Hearn W, Elsworth J, Roth R, Bradberry C, Taylor J. Cocaethylene inhibits uptake of dopamine and can reach high plasma concentrations following combined cocaine and ethanol use. NIDA Research Monograph 1990, 105: 572-3. PMID: 1876124.Peer-Reviewed Original Research