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 aspectsCortexRecapitulation and Reversal of a Persistent Depression‐like Syndrome in Rodents
Gourley SL, Taylor JR. Recapitulation and Reversal of a Persistent Depression‐like Syndrome in Rodents. Current Protocols In Neuroscience 2009, 49: 9.32.1-9.32.11. PMID: 19802817, PMCID: PMC2774936, DOI: 10.1002/0471142301.ns0932s49.Peer-Reviewed Original ResearchConceptsCORT exposureChronic mild stress modelChronic antidepressant treatmentChronic CORT exposureHelplessness-like behaviorDepressive-like stateNeurobiology of depressionDepression-like syndromeChronic oral exposureAntidepressant efficacyAntidepressant treatmentAdrenal hormonesOral exposureNucleus accumbensMouse modelFeelings of anhedoniaNaïve rodentsMultiple biological functionsMolecular targetsCAMP response elementDepressionFactor activityCorticosteroneExposure periodExposure
2008
Corticosterone Regulates pERK1/2 Map Kinase in a Chronic Depression Model
Gourley SL, Wu FJ, Taylor JR. Corticosterone Regulates pERK1/2 Map Kinase in a Chronic Depression Model. Annals Of The New York Academy Of Sciences 2008, 1148: 509-514. PMID: 19120149, PMCID: PMC3657205, DOI: 10.1196/annals.1410.076.Peer-Reviewed Original ResearchConceptsDepression modelCA1/CA3Chronic depression modelPrefrontal cortical targetsExtracellular signal-regulated kinase 1/2Signal-regulated kinase 1/2Antidepressant efficacyDentate gyrusCorticosterone exposureCortical targetsReceptor typesKinase 1/2Motivated behaviorNovel roleIntracellular signalingPERK1/2MAP kinaseTranscriptional activityNeurotrophinsHippocampusCorticosteroneCA3GyrusMiceInsult
2007
Regionally Specific Regulation of ERK MAP Kinase in a Model of Antidepressant-Sensitive Chronic Depression
Gourley SL, Wu FJ, Kiraly DD, Ploski JE, Kedves AT, Duman RS, Taylor JR. Regionally Specific Regulation of ERK MAP Kinase in a Model of Antidepressant-Sensitive Chronic Depression. Biological Psychiatry 2007, 63: 353-359. PMID: 17889834, PMCID: PMC2277331, DOI: 10.1016/j.biopsych.2007.07.016.Peer-Reviewed Original ResearchMeSH KeywordsAmitriptylineAnimalsAntidepressive Agents, TricyclicAnti-Inflammatory AgentsChronic DiseaseConditioning, OperantCorticosteroneCREB-Binding ProteinDentate GyrusDepressive Disorder, MajorDisease Models, AnimalEndoplasmic Reticulum Chaperone BiPExtracellular Signal-Regulated MAP KinasesFluoxetineHeat-Shock ProteinsHippocampusLocomotionMiceMice, Inbred C57BLMolecular ChaperonesMotivationSelective Serotonin Reuptake InhibitorsConceptsAntidepressant efficacyChronic corticosteroneDentate gyrusChronic depressionCA1/CA3Depression-like behaviorExtracellular signal-regulated kinase 1/2Response element-binding proteinSignal-regulated kinase 1/2Amitriptyline treatmentGlucocorticoid exposureADT treatmentNaive rodentsBehavioral despairLong-term consequencesTail suspensionElement-binding proteinCyclic adenosine monophosphateBiochemical measuresERK MAP kinasePrefrontal cortexHeat shock proteinsOperant conditioning taskCommon mediatorPERK1/2
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) model
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 studyDeficitsUpregulation of striatal D2 receptors in the MPTP-treated vervet monkey is reversed by grafts of fetal ventral mesencephalon: an autoradiographic study
Elsworth J, Brittan M, Taylor J, Sladek J, Redmond D, Innis R, Zea-Ponce Y, Roth R. Upregulation of striatal D2 receptors in the MPTP-treated vervet monkey is reversed by grafts of fetal ventral mesencephalon: an autoradiographic study. Brain Research 1998, 795: 55-62. PMID: 9622593, DOI: 10.1016/s0006-8993(98)00252-2.Peer-Reviewed Original ResearchMeSH Keywords1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineAnimalsAutoradiographyBenzofuransBrain Tissue TransplantationChlorocebus aethiopsCorpus StriatumDisease Models, AnimalDopamine AgentsFetal Tissue TransplantationImage Processing, Computer-AssistedIodine RadioisotopesMesencephalonParkinson Disease, SecondaryRadioligand AssayReceptors, Dopamine D2Up-RegulationConceptsFetal ventral mesencephalonD2 receptor bindingVentral mesencephalonDorsal striatumAutoradiographic studyDopamine uptake site densityPostsynaptic dopamine receptor activationVentral striatumDopamine concentrationsStriatal D2 receptor bindingReceptor bindingD2 receptor upregulationPostsynaptic dopamine transmissionTetrahydropyridine-treated monkeysStriatal D2 receptorsDopamine receptor activationPrevious autoradiographic studiesAfrican green monkeysDonor neuronsIntrastriatal graftingParkinsonian primatesNeural transplantationReceptor upregulationStriatal circuitryMotor functionPattern of synaptophysin immunoreactivity within mesencephalic grafts following transplantation in a parkinsonian primate model
Sortwell C, Blanchard B, Collier T, Elsworth J, Taylor J, Roth R, Redmond D, Sladek J. Pattern of synaptophysin immunoreactivity within mesencephalic grafts following transplantation in a parkinsonian primate model. Brain Research 1998, 791: 117-124. PMID: 9593853, DOI: 10.1016/s0006-8993(98)00086-9.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCercopithecusDisease Models, AnimalFetal Tissue TransplantationImmunohistochemistryMaleMesencephalonParkinson Disease, SecondarySynaptophysinConceptsGraft-host interactionsMesencephalic graftsFunctional synapsesTyrosine hydroxylaseCerebellar tissuePericellular arraysEmbryonic cerebellar tissueEmbryonic ventral mesencephalonGrafted dopamine neuronsNerve terminal differentiationTH-positive neuronsStriatum of MPTPEnzyme tyrosine hydroxylaseSynthetic enzyme tyrosine hydroxylaseAfrican green monkeysNeurochemical subtypesStriatal portionDA neuronsSynaptophysin immunoreactivityVentral mesencephalonGraft typeDopamine neuronsPrimate modelStriatal targetsSynaptic remodeling
1997
Enduring Cognitive Deficits and Cortical Dopamine Dysfunction in Monkeys After Long-Term Administration of Phencyclidine
Jentsch J, Redmond D, Elsworth J, Taylor J, Youngren K, Roth R. Enduring Cognitive Deficits and Cortical Dopamine Dysfunction in Monkeys After Long-Term Administration of Phencyclidine. Science 1997, 277: 953-955. PMID: 9252326, DOI: 10.1126/science.277.5328.953.Peer-Reviewed Original ResearchConceptsDopamine utilizationPrefrontal cortexAtypical antipsychotic drug clozapineLong-term administrationDirect drug effectAntipsychotic drug clozapinePsychotomimetic drug phencyclidineAdministration of phencyclidineDorsolateral prefrontal cortexDopamine hypofunctionPrefrontal cortex functionCognitive dysfunctionPhencyclidine treatmentBehavioral deficitsDopamine dysfunctionPsychiatric disordersDrug effectsDrug clozapineDrug phencyclidineBrain regionsCognitive deficitsCortex functionCognitive functionPhencyclidineCortex
1995
Sham surgery does not ameliorate MPTP-induced behavioral deficits in monkeys
Taylor J, Elsworth J, Sladek J, Collier T, Roth R, Redmond D. Sham surgery does not ameliorate MPTP-induced behavioral deficits in monkeys. Cell Transplantation 1995, 4: 13-26. DOI: 10.1016/0963-6897(94)00035-i.Peer-Reviewed Original ResearchConceptsFetal mesencephalic tissueSubstantia nigra graftsSham surgeryBehavioral improvementMesencephalic tissueBehavioral deficitsAdult male African green monkeysDopamine concentrationsMale African green monkeysFetal dopamine neuronsSystemic MPTP administrationIdiopathic Parkinson's diseaseStriatum of MPTPSham-operated monkeysPostmortem brain tissueAfrican green monkeysMore variable effectsNeuronal synaptic connectionsHost neuronsHost striatumHost brainMPTP administrationGestational ageSubstantia nigraNeuronal effectsSham Surgery does not Ameliorate MPTP-Induced Behavioral Deficits in Monkeys
Taylor J, Elsworth J, Sladek J, Collier T, Roth R, Redmond D. Sham Surgery does not Ameliorate MPTP-Induced Behavioral Deficits in Monkeys. Cell Transplantation 1995, 4: 13-26. PMID: 7728327, DOI: 10.1177/096368979500400105.Peer-Reviewed Original ResearchConceptsFetal mesencephalic tissueSubstantia nigra graftsSham surgeryBehavioral improvementMesencephalic tissueBehavioral deficitsAdult male African green monkeysDopamine concentrationsMale African green monkeysFetal dopamine neuronsSystemic MPTP administrationIdiopathic Parkinson's diseaseStriatum of MPTPSham-operated monkeysPostmortem brain tissueAfrican green monkeysMore variable effectsNeuronal synaptic connectionsHost neuronsHost striatumHost brainMPTP administrationGestational ageSubstantia nigraNeuronal effects
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 animalsMPTP
1990
Chapter 62 Improvements in MPTP-induced object retrieval deficits and behavioral deficits after fetal nigral grafting in monkeys
Taylor J, Elsworth J, Roth R, Collier T, Sladek J, Redmond D. Chapter 62 Improvements in MPTP-induced object retrieval deficits and behavioral deficits after fetal nigral grafting in monkeys. Progress In Brain Research 1990, 82: 543-559. PMID: 2290957, DOI: 10.1016/s0079-6123(08)62645-x.Peer-Reviewed Original ResearchConceptsCSF HVA levelsHVA levelsBehavioral recoveryCaudate nucleusSN graftsDopamine neuronsDopamine productionHVA/dopamine ratioCentral dopamine productionFetal substantia nigraStriatum of subjectsSubstantia nigra transplantsRelease of dopamineImproved parkinsonismHost striatumHost brainFetal graftsMPTP administrationParkinsonian signsTH immunohistochemistrySubstantia nigraDopamine ratioSmall graftsBehavioral deficitsGraft