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 ResearchConceptsPosttraumatic 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 miceThe effects of fatty acid amide hydrolase inhibition and monoacylglycerol lipase inhibition on habit formation in mice
Gianessi CA, Groman SM, Taylor JR. The effects of fatty acid amide hydrolase inhibition and monoacylglycerol lipase inhibition on habit formation in mice. European Journal Of Neuroscience 2021, 55: 922-938. PMID: 33506530, PMCID: PMC10370500, DOI: 10.1111/ejn.15129.Peer-Reviewed Original ResearchConceptsFatty acid amide hydrolase inhibitionResponse rateHydrolase inhibitionCannabinoid receptor type 1Aberrant habit formationInhibition of FAAHMonoacylglycerol lipase inhibitionInconsistent dose-response relationshipRole of CB1RSubstance use disordersEndocannabinoid ligand anandamideReceptor type 1Dose-response relationshipContingency degradation procedureEndocannabinoid signalingClinical utilityAM251Use disordersType 1Behavioral effectsPharmacological compoundsDose-response experimentsMiceLipase inhibitionAnandamide
1998
In vivo expression of therapeutic human genes for dopamine production in the caudates of MPTP-treated monkeys using an AAV vector
During M, Samulski R, Elsworth J, Kaplitt M, Leone P, Xiao X, Li J, Freese A, Taylor J, Roth R, Sladek J, O’Malley K, Redmond D. In vivo expression of therapeutic human genes for dopamine production in the caudates of MPTP-treated monkeys using an AAV vector. Gene Therapy 1998, 5: 820-827. PMID: 9747462, DOI: 10.1038/sj.gt.3300650.Peer-Reviewed Original ResearchMeSH Keywords1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineAnimalsAromatic-L-Amino-Acid DecarboxylasesChlorocebus aethiopsDependovirusDopamineDopamine AgentsGene ExpressionGene Transfer TechniquesGenetic VectorsHumansImmunohistochemistryMaleParkinson DiseaseTrigeminal Caudal NucleusTyrosine 3-MonooxygenaseConceptsTyrosine hydroxylaseStriatal cellsDopamine-depleted monkeysAdeno-associated virus vectorProduction of dopamineParkinsonian monkeysTransient feverSevere hyperactivityStriatal dopaminePrimate neuronsStereotactic injectionHistological evidencePrimate modelInjection tractNeurotoxin MPTPDopamine productionParkinson's diseaseTreatment groupsSignificant toxicityBehavioral effectsVivo gene therapyElevated levelsBiochemical effectsFirst dayMonkeys
1997
Dysregulation of Mesoprefrontal Dopamine Neurons Induced by Acute and Repeated Phencyclidine Administration in the Nonhuman Primate: Implications for Schizophrenia
Jentsch J, Elsworth J, Taylor J, Redmond D, Roth R. Dysregulation of Mesoprefrontal Dopamine Neurons Induced by Acute and Repeated Phencyclidine Administration in the Nonhuman Primate: Implications for Schizophrenia. Advances In Pharmacology 1997, 42: 810-814. PMID: 9328021, DOI: 10.1016/s1054-3589(08)60870-4.Peer-Reviewed Original ResearchConceptsPCP administrationAcute PCP administrationNegative symptomsDA systemMesoprefrontal dopamine neuronsSubcortical DA systemsBrains of patientsSchizophrenia-like symptomatologyDevelopment of neuropathologyDistinct behavioral effectsDAergic dysfunctionDA metabolismDAergic functionDopamine neuronsCognitive dysfunctionNovel agentsDeficits of schizophreniaFrontal cortexPsychotomimetic propertiesNeurobiological effectsDopamine systemPositive symptomsPhencyclidine administrationBehavioral effectsAdministration
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 area
1993
Serotonin involvement in cocaine sensitization: Clues from studies with cocaine analogs
Elsworth J, Taylor J, Jatlow P, Roth R. Serotonin involvement in cocaine sensitization: Clues from studies with cocaine analogs. Drug Development Research 1993, 30: 189-200. DOI: 10.1002/ddr.430300311.Peer-Reviewed Original ResearchLocomotor activityAcute dose-response studySubsequent challenge doseΒ-CITCentral dopamine systemsInhibitor of serotoninDopamine uptake sitesCocaine-induced sensitizationInhibitors of dopamineDose-response studyUptake of dopamineRat locomotor activitySerotonin componentConcurrent ingestionChallenge doseSerotonin uptakeNorepinephrine uptakeSerotonergic systemChronic cocaineDopamine systemDopamine uptakeCocaine actionUptake sitesBehavioral effectsComparative potency
1991
Cocaethylene: 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