2001
Neurotrophin-3 modulates noradrenergic neuron function and opiate withdrawal
Akbarian S, Bates B, Liu R, Skirboll S, Pejchal T, Coppola V, Sun L, Fan G, Kucera J, Wilson M, Tessarollo L, Kosofsky B, Taylor J, Bothwell M, Nestler E, Aghajanian G, Jaenisch R. Neurotrophin-3 modulates noradrenergic neuron function and opiate withdrawal. Molecular Psychiatry 2001, 6: 593-604. PMID: 11526474, DOI: 10.1038/sj.mp.4000897.Peer-Reviewed Original ResearchMeSH KeywordsAgingAnimalsAvoidance LearningBrainColforsinCyclic AMPElectric StimulationEnkephalin, Ala(2)-MePhe(4)-Gly(5)-Gene Expression Regulation, EnzymologicIn Vitro TechniquesIntermediate Filament ProteinsLocus CoeruleusMiceMice, KnockoutMice, TransgenicMorphineMorphine DependenceNerve Tissue ProteinsNestinNeuronsNeurotrophin 3Signal TransductionSubstance Withdrawal SyndromeTyrosine 3-MonooxygenaseConceptsNoradrenergic neuronsNeurotrophin-3NT-3Opiate withdrawalNoradrenergic signalingOpiate withdrawal symptomsChronic morphine exposureNT-3 expressionNon-catecholaminergic neuronsLoss of neuronsDorsal medullaMorphine exposureWithdrawal symptomsAfferent sourcesTyrosine hydroxylaseAdult brainSomatic symptomsNeuron functionVentral forebrainConditional ablationReduced upregulationNeuronsAltered cAMPSymptomsWithdrawalEffects 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 neurons
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 studyDeficits
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
1988
Chapter 64 Fetal dopamine neural grafts: extended reversal of methylphenyltetrahydropyridine-induced parkinsonism in monkeys
Sladek J, Redmond D, Collier T, Blount J, Elsworth J, Taylor J, Roth R. Chapter 64 Fetal dopamine neural grafts: extended reversal of methylphenyltetrahydropyridine-induced parkinsonism in monkeys. Progress In Brain Research 1988, 78: 497-506. PMID: 3266802, DOI: 10.1016/s0079-6123(08)60323-4.Peer-Reviewed Original ResearchConceptsDopamine neuronsTherapeutic interventionsHuman parkinsonismHost brainFunctional recoveryDopaminergic neuronsSubstantia nigraCell graftsDopamine levelsFetal brainGraft siteTrophic factorsHuman neuronsAnatomical substrateParkinsonismCerebellar tissueControl transplantsNeuronsGraftBrain activityPhenotype characteristicBrainInterventionTransplantationTransplant
1984
Enhanced behavioural control by conditioned reinforcers following microinjections of d-amphetamine into the nucleus accumbens
Taylor J, Robbins T. Enhanced behavioural control by conditioned reinforcers following microinjections of d-amphetamine into the nucleus accumbens. Psychopharmacology 1984, 84: 405-412. PMID: 6440188, DOI: 10.1007/bf00555222.Peer-Reviewed Original Research