Featured Publications
Positive modulation of N-methyl-D-aspartate receptors in the mPFC reduces the spontaneous recovery of fear
Lee B, Pothula S, Wu M, Kang H, Girgenti MJ, Picciotto MR, DiLeone RJ, Taylor JR, Duman RS. Positive modulation of N-methyl-D-aspartate receptors in the mPFC reduces the spontaneous recovery of fear. Molecular Psychiatry 2022, 27: 2580-2589. PMID: 35418600, PMCID: PMC9135632, DOI: 10.1038/s41380-022-01498-7.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsExtinction, PsychologicalFearMaleMicePrefrontal CortexRatsRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateConceptsPosttraumatic stress disorderFear extinctionInfralimbic medial prefrontal cortexFear conditioning modelEnhanced fear extinctionFear-based behaviorsProlonged stress modelMedial prefrontal cortexSpontaneous recoveryIL-mPFCPTSD modelPTSD treatmentStress disorderPrefrontal cortexSPS modelN-methyl-D-aspartate receptor modulatorsBrain-derived neurotrophic factorN-methyl-D-aspartate receptorsBehavioral effectsIncreased attentionMPFCPreclinical findingsPyramidal neuronsNeurotrophic factorMale mice
2009
Neuronal Correlates of Instrumental Learning in the Dorsal Striatum
Kimchi EY, Torregrossa MM, Taylor JR, Laubach M. Neuronal Correlates of Instrumental Learning in the Dorsal Striatum. Journal Of Neurophysiology 2009, 102: 475-489. PMID: 19439679, PMCID: PMC2712266, DOI: 10.1152/jn.00262.2009.Peer-Reviewed Original ResearchConceptsDorsal striatumResponse portsNeuronal activityTask-related firingTask-related neuronsMovement-related potentialsInitiation of movementLateral striatumLearning-related changesMedial striatumStriatumNeuronal correlatesReward portNumber of neuronsAcoustic stimuliNeuronsOperant taskField potentialsProgressive increaseLateral regionsTheta-band oscillationsHigh rateTraining periodInstrumental learningHead entries
2008
A History of Corticosterone Exposure Regulates Fear Extinction and Cortical NR2B, GluR2/3, and BDNF
Gourley SL, Kedves AT, Olausson P, Taylor JR. A History of Corticosterone Exposure Regulates Fear Extinction and Cortical NR2B, GluR2/3, and BDNF. Neuropsychopharmacology 2008, 34: 707-716. PMID: 18719621, PMCID: PMC3679657, DOI: 10.1038/npp.2008.123.Peer-Reviewed Original ResearchConceptsPosttraumatic stress disorderConditioned fearFear memory acquisitionFear extinction trainingVentromedial prefrontal cortexContextual fear conditioningMedial orbitofrontal cortexPrior chronic exposureExtinction learningFear extinctionExtinction trainingFear conditioningFear statesImpairs extinctionStress disorderBehavioral flexibilityMemory acquisitionOrbitofrontal cortexPrefrontal cortexNeural systemsAMPA receptor subunitsCortical regionsActive learning processPrior stressGlucocorticoid exposure
2005
Persistent changes in motivation to self‐administer cocaine following modulation of cyclic AMP‐dependent protein kinase A (PKA) activity in the nucleus accumbens
Lynch W, Taylor J. Persistent changes in motivation to self‐administer cocaine following modulation of cyclic AMP‐dependent protein kinase A (PKA) activity in the nucleus accumbens. European Journal Of Neuroscience 2005, 22: 1214-1220. PMID: 16176364, DOI: 10.1111/j.1460-9568.2005.04305.x.Peer-Reviewed Original Research
2001
Repeated intermittent administration of psychomotor stimulant drugs alters the acquisition of Pavlovian approach behavior in rats: differential effects of cocaine, d-amphetamine and 3,4-methylenedioxymethamphetamine (“ecstasy”)
Taylor J, Jentsch J. Repeated intermittent administration of psychomotor stimulant drugs alters the acquisition of Pavlovian approach behavior in rats: differential effects of cocaine, d-amphetamine and 3,4-methylenedioxymethamphetamine (“ecstasy”). Biological Psychiatry 2001, 50: 137-143. PMID: 11526995, DOI: 10.1016/s0006-3223(01)01106-4.Peer-Reviewed Original ResearchEffects of chronic exposure to cocaine are regulated by the neuronal protein Cdk5
Bibb J, Chen J, Taylor J, Svenningsson P, Nishi A, Snyder G, Yan Z, Sagawa Z, Ouimet C, Nairn A, Nestler E, Greengard P. Effects of chronic exposure to cocaine are regulated by the neuronal protein Cdk5. Nature 2001, 410: 376-380. PMID: 11268215, DOI: 10.1038/35066591.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBrainCocaineCocaine-Related DisordersCorpus StriatumCyclin-Dependent Kinase 5Cyclin-Dependent KinasesDopamineDopamine and cAMP-Regulated Phosphoprotein 32Enzyme InhibitorsGene Expression Regulation, EnzymologicKinetinMaleMiceMice, TransgenicNerve Tissue ProteinsNeuronsOligonucleotide Array Sequence AnalysisPhosphoproteinsPhosphorylationProto-Oncogene Proteins c-fosPsychomotor PerformancePurinesRatsRats, Sprague-DawleyReceptors, Dopamine D1RoscovitineSignal TransductionConceptsTranscription factorsSuch transcription factorsDownstream target genesCyclin-dependent kinase 5DNA array analysisTarget genesGene expressionCocaine administrationKinase 5Inducible transgenic miceChronic exposureCdk5 inhibitorMessenger RNACocaine addictionArray analysisDopamine-mediated neurotransmissionDopamine-containing nerve terminalsMedium spiny neuronsD1 dopamine receptorsChronic cocaine administrationOverexpression of ΔFosBProteinTransgenic miceAdaptive changesSpiny neuronsImpaired Inhibition of Conditioned Responses Produced by Subchronic Administration of Phencyclidine to Rats
Jentsch J, Taylor J. Impaired Inhibition of Conditioned Responses Produced by Subchronic Administration of Phencyclidine to Rats. Neuropsychopharmacology 2001, 24: 66-74. PMID: 11106877, DOI: 10.1016/s0893-133x(00)00174-3.Peer-Reviewed Original ResearchConceptsPCP-treated ratsStimulus-reward associationsNovel instrumental responseInhibitory response controlObsessive-compulsive disorderMore responsesConcurrent discriminationReversal learningFrontostriatal systemIncentive stimuliAffective impairmentsInhibitory controlInstrumental respondingImpaired inhibitionConditioned responseInstrumental responsePCP treatmentResponse controlMental disordersCurrent studyDrug abuseStimuliLearningSubchronic administrationImpulsivity
1999
A role for norepinephrine in stress-induced cognitive deficits: α-1-adrenoceptor mediation in the prefrontal cortex
Birnbaum S, Gobeske K, Auerbach J, Taylor J, Arnsten A. A role for norepinephrine in stress-induced cognitive deficits: α-1-adrenoceptor mediation in the prefrontal cortex. Biological Psychiatry 1999, 46: 1266-1274. PMID: 10560032, DOI: 10.1016/s0006-3223(99)00138-9.Peer-Reviewed Original ResearchConceptsStress-induced cognitive deficitsPoor attention regulationAlternation performanceSpatial working memoryPFC cognitive functionPrefrontal cortical dysfunctionMotor response timeIntra-PFC infusionsStress-induced deficitsStress-induced impairmentWorking memoryAttention regulationPFC contributeMemory performanceAlternation testingStress researchNeuropsychiatric disordersPrefrontal cortexCognitive deficitsCognitive functionMemory functionMemory impairmentPFC dysfunctionPerseverative patternsPharmacological stressorEnhancement 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 associationsα-1 noradrenergic receptor stimulation impairs prefrontal cortical cognitive function
Arnsten A, Mathew R, Ubriani R, Taylor J, Li B. α-1 noradrenergic receptor stimulation impairs prefrontal cortical cognitive function. Biological Psychiatry 1999, 45: 26-31. PMID: 9894572, DOI: 10.1016/s0006-3223(98)00296-0.Peer-Reviewed Original ResearchConceptsPrefrontal cortexCognitive functionPrefrontal cortical cognitive functionCortical cognitive functionsImpairs cognitive functionHigher cortical functionsMemory taskAlpha-1 adrenoceptorsMost antipsychotic medicationsAlternation performanceNoradrenergic turnoverCortical functionPhenylephrine responseAlpha-1 adrenoceptor stimulationNeuropsychiatric disordersAlpha-1 adrenergic antagonistAlpha-1 adrenergic agonistDisordersAntipsychotic medicationAnxietyHigh levelsPhenylephrine infusionAdrenoceptor stimulationAdrenergic antagonistsSecond messenger pathways
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 studyDeficitsA comparison of the effects of clonidine and CNQX infusion into the locus coeruleus and the amygdala on naloxone-precipitated opiate withdrawal in the rat
Taylor J, Punch L, Elsworth J. A comparison of the effects of clonidine and CNQX infusion into the locus coeruleus and the amygdala on naloxone-precipitated opiate withdrawal in the rat. Psychopharmacology 1998, 138: 133-142. PMID: 9718282, DOI: 10.1007/s002130050655.Peer-Reviewed Original ResearchPrefrontal 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 bindingSupranormal Stimulation of D1 Dopamine Receptors in the Rodent Prefrontal Cortex Impairs Spatial Working Memory Performance
Zahrt J, Taylor J, Mathew R, Arnsten A. Supranormal Stimulation of D1 Dopamine Receptors in the Rodent Prefrontal Cortex Impairs Spatial Working Memory Performance. Journal Of Neuroscience 1997, 17: 8528-8535. PMID: 9334425, PMCID: PMC6573725, DOI: 10.1523/jneurosci.17-21-08528.1997.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBenzazepinesDopamineDopamine AgonistsDopamine AntagonistsInfusions, ParenteralMaleMaze LearningMemoryModels, NeurologicalModels, PsychologicalPrefrontal CortexPsychomotor PerformanceRatsRats, Sprague-DawleyReceptors, Dopamine D1Receptors, N-Methyl-D-AspartateSpatial BehaviorStress, PsychologicalConceptsD1 receptor stimulationPrefrontal cortexReceptor stimulationSKF 81297SCH 23390D1 receptorsSupranormal stimulationPFC of ratsD1 receptor mechanismsDA receptor stimulationDose-related impairmentD1 receptor antagonistD1 receptor agonistD1 dopamine receptorsDelayed-alternation performanceMemory functionRecent electrophysiological studiesSpatial Working Memory PerformanceReceptor antagonistReceptor agonistDopamine receptorsReceptor mechanismsElectrophysiological studiesHigh dosesDrug efficacy
1996
Sensitization to the locomotor activating effects of cocaine following cocaethylene-preexposure
Horger B, Taylor J, Elsworth J, Jatlow P, Roth R. Sensitization to the locomotor activating effects of cocaine following cocaethylene-preexposure. Brain Research 1996, 733: 133-137. PMID: 8891259, DOI: 10.1016/0006-8993(96)00783-4.Peer-Reviewed Original Research
1995
Prior exposure to cocaine diminishes behavioral and biochemical responses to aversive conditioning: Reversal by glycine/N-methyl-d-aspartate antagonist co-treatment
Morrow B, Taylor J, Roth R. Prior exposure to cocaine diminishes behavioral and biochemical responses to aversive conditioning: Reversal by glycine/N-methyl-d-aspartate antagonist co-treatment. Neuroscience 1995, 69: 233-240. PMID: 8637621, DOI: 10.1016/0306-4522(95)00184-k.Peer-Reviewed Original ResearchConceptsAversive conditioningAversive conditioning paradigmMedial prefrontal cortexCocaine-exposed groupNeutral stimuliConditioned fearConditioning paradigmPrefrontal cortexHA-966Conditioning sessionsPrior exposureStressful effectsLocomotor stimulant propertiesBehavioral effectsFootshockConditioningN-methyl-D-aspartate antagonistsStressful stimuliAmount of timeFearStimuliN-methyl-D-aspartate (NMDA) receptor complexDoses of cocaineSessionsVentral tegmental areaR-(+)-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