2009
Recapitulation 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
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 stressor
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
1997
(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