2016
Evaluation of the Nicotinic Acetylcholine Receptor-Associated Proteome at Baseline and Following Nicotine Exposure in Human and Mouse Cortex
McClure-Begley TD, Esterlis I, Stone KL, Lam TT, Grady SR, Colangelo CM, Lindstrom JM, Marks MJ, Picciotto MR. Evaluation of the Nicotinic Acetylcholine Receptor-Associated Proteome at Baseline and Following Nicotine Exposure in Human and Mouse Cortex. ENeuro 2016, 3: eneuro.0166-16.2016. PMID: 27559543, PMCID: PMC4985585, DOI: 10.1523/eneuro.0166-16.2016.Peer-Reviewed Original ResearchConceptsPutative interacting proteinsQuantitative proteomic assessmentProtein-protein interactionsTemporal cortex tissueChaperone familyMood disordersInteracting proteinProtein complexesPresynaptic neurotransmitter releaseNovel etiological mechanismsNicotine exposureProteomic assessmentProteomeNicotinic acetylcholine receptorsMouse cortexProteinHigh-affinity nAChRsΒ2 subunitCortex of miceMaintenance of smokingNew treatment targetsResult of smokingNeurotransmitter releaseAcetylcholine receptorsPrimary function
2013
High-affinity nicotinic acetylcholine receptor expression and trafficking abnormalities in psychiatric illness
Lewis AS, Picciotto MR. High-affinity nicotinic acetylcholine receptor expression and trafficking abnormalities in psychiatric illness. Psychopharmacology 2013, 229: 477-485. PMID: 23624811, PMCID: PMC3766461, DOI: 10.1007/s00213-013-3126-5.Peer-Reviewed Original ResearchConceptsPsychiatric illnessNicotinic acetylcholine receptor expressionPre-clinical animal modelsMultiple psychiatric illnessesChronic nicotine exposureHigh-affinity nAChRsAcetylcholine receptor expressionNicotinic receptor subtypesNovel therapeutic agentsHuman psychiatric illnessCholinergic dysfunctionClinical featuresNicotine exposurePatient populationCholinergic systemNicotine intakeReceptor expressionReceptor subtypesMood disordersTobacco usePharmacological agentsAnimal modelsPsychiatric diseasesAcetylcholine receptorsIllness
2009
Localized low‐level re‐expression of high‐affinity mesolimbic nicotinic acetylcholine receptors restores nicotine‐induced locomotion but not place conditioning
Mineur YS, Brunzell DH, Grady SR, Lindstrom JM, McIntosh JM, Marks MJ, King SL, Picciotto MR. Localized low‐level re‐expression of high‐affinity mesolimbic nicotinic acetylcholine receptors restores nicotine‐induced locomotion but not place conditioning. Genes Brain & Behavior 2009, 8: 257-266. PMID: 19077117, PMCID: PMC2672109, DOI: 10.1111/j.1601-183x.2008.00468.x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsConditioning, PsychologicalCyclic AMP Response Element-Binding ProteinDopamineGamma-Aminobutyric AcidGene Expression RegulationLocomotionMiceMice, Inbred C57BLMice, TransgenicNicotineNicotinic AgonistsPhosphorylationPresynaptic TerminalsReceptors, NicotinicRewardSynaptosomesTobacco Use DisorderVentral Tegmental AreaConceptsVentral tegmental areaGamma-aminobutyric acidNicotinic acetylcholine receptorsCyclic AMP response element binding proteinTegmental areaPlace preferenceTransgenic miceAcetylcholine receptorsBeta2 knockout micePedunculopontine tegmental areaSystemic nicotine administrationHigh-affinity nAChRsLaterodorsal tegmental nucleusNicotine place preferenceNicotinic partial agonistPlace preference testingDifferent neuronal subtypesAMP response element binding proteinTotal CREB levelsResponse element-binding proteinDA neuronsCholinergic neuronsNicotine administrationSystemic nicotineSmoking cessation
2004
High-affinity nicotinic acetylcholine receptors are required for antidepressant effects of amitriptyline on behavior and hippocampal cell proliferation
Caldarone BJ, Harrist A, Cleary MA, Beech RD, King SL, Picciotto MR. High-affinity nicotinic acetylcholine receptors are required for antidepressant effects of amitriptyline on behavior and hippocampal cell proliferation. Biological Psychiatry 2004, 56: 657-664. PMID: 15522249, DOI: 10.1016/j.biopsych.2004.08.010.Peer-Reviewed Original ResearchMeSH KeywordsAmitriptylineAnalysis of VarianceAnimalsAntidepressive Agents, TricyclicBehavior, AnimalBromodeoxyuridineCell CountCell ProliferationDose-Response Relationship, DrugDrosophila ProteinsDrug InteractionsHelplessness, LearnedHindlimb SuspensionHippocampusImmunohistochemistryMecamylamineMiceMice, Inbred C57BLMice, KnockoutNeuronsNicotinic AntagonistsNortriptylineReceptors, NicotinicSwimmingConceptsHigh-affinity nAChRsHippocampal cell proliferationNicotinic acetylcholine receptorsSwim testAcetylcholine receptorsCell proliferationHigh-affinity nicotinic acetylcholine receptorsNoncompetitive nAChR antagonist mecamylamineAntagonism of nAChRsAntidepressant-induced increasesAntidepressant-like effectsNAChR antagonist mecamylamineWild-type miceInhibition of nAChRsAntidepressants actAntidepressant actionAntidepressant effectsChronic treatmentAntagonist mecamylamineAntidepressant propertiesTricyclic antidepressantsAntidepressant activityTherapeutic effectKnockout miceNoncompetitive antagonist
2003
Conditional Expression in Corticothalamic Efferents Reveals a Developmental Role for Nicotinic Acetylcholine Receptors in Modulation of Passive Avoidance Behavior
King SL, Marks MJ, Grady SR, Caldarone BJ, Koren AO, Mukhin AG, Collins AC, Picciotto MR. Conditional Expression in Corticothalamic Efferents Reveals a Developmental Role for Nicotinic Acetylcholine Receptors in Modulation of Passive Avoidance Behavior. Journal Of Neuroscience 2003, 23: 3837-3843. PMID: 12736354, PMCID: PMC6742204, DOI: 10.1523/jneurosci.23-09-03837.2003.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAvoidance LearningBehavior, AnimalBinding, CompetitiveCerebral CortexElectroshockGene Expression Regulation, DevelopmentalMiceMice, Inbred C57BLMice, Inbred ICRMice, KnockoutMice, TransgenicNeurons, EfferentNicotineNicotinic AgonistsPresynaptic TerminalsReceptors, NicotinicTetracyclineThalamusTransgenesConceptsPrenatal nicotine exposureNicotinic acetylcholine receptorsPassive avoidanceLines of miceNicotine exposureTransgenic miceAcetylcholine receptorsHigh-affinity nicotinic acetylcholine receptorsTetracycline-regulated transgenic systemHigh-affinity nicotinic receptorsPotential neuroanatomical substratesRubidium efflux assaysHigh-affinity nAChRsEffects of nicotineSpecific neuronal populationsPassive avoidance behaviorAttention deficit hyperactivity disorderWild-type animalsDeficit hyperactivity disorderPresynaptic nAChRsCorticothalamic neuronsSite of actionNicotinic receptorsNeuronal populationsCognitive impairment
2001
Nicotine Receptor Inactivation Decreases Sensitivity to Cocaine
Zachariou V, Caldarone B, Weathers-Lowin A, George T, Elsworth J, Roth R, Changeux J, Picciotto M. Nicotine Receptor Inactivation Decreases Sensitivity to Cocaine. Neuropsychopharmacology 2001, 24: 576-589. PMID: 11282258, DOI: 10.1016/s0893-133x(00)00224-4.Peer-Reviewed Original ResearchConceptsPlace preferenceDA turnoverLow doseHigh-affinity nicotinic acetylcholine receptorsMesolimbic DA systemHigh-affinity nAChRsNicotinic antagonist mecamylamineWild-type miceMesolimbic dopamine systemFos-related antigensProperties of nicotineCocaine place preferenceΒ2 subunitNicotinic acetylcholine receptorsAntagonist mecamylamineDA releaseMetabolite DOPACNeurochemical changesSubthreshold doseType miceDopamine systemPsychomotor stimulantsAcetylcholine receptorsHigh dosesBrain regions