1999
Altered frontal cortical dopaminergic transmission in monkeys after subchronic phencyclidine exposure: involvement in frontostriatal cognitive deficits
Jentsch J, Taylor J, Elsworth J, Redmond D, Roth R. Altered frontal cortical dopaminergic transmission in monkeys after subchronic phencyclidine exposure: involvement in frontostriatal cognitive deficits. Neuroscience 1999, 90: 823-832. PMID: 10218783, DOI: 10.1016/s0306-4522(98)00481-3.Peer-Reviewed Original ResearchConceptsCognitive deficitsSubchronic phencyclidine administrationDorsolateral prefrontal cortexFrontal cortexCortical dopamine transmissionReduced dopaminergic functionFrontostriatal functionDetour taskCognitive performanceDopamine utilizationPhencyclidine exposurePrefrontal cortexPerformance impairmentPrelimbic cortexBrain regionsCognitive dysfunctionCortical impairmentCortical regionsCognitive impairmentDopaminergic functionPhencyclidine administrationDopamine transmissionSpecific subregionsCortexPsychotomimetic drug phencyclidine
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 studyDeficitsPrefrontal 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
(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 bindingEnduring 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