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
2010
Cortico-Thalamic Connectivity is Vulnerable to Nicotine Exposure During Early Postnatal Development through α4/β2/α5 Nicotinic Acetylcholine Receptors
Heath CJ, King SL, Gotti C, Marks MJ, Picciotto MR. Cortico-Thalamic Connectivity is Vulnerable to Nicotine Exposure During Early Postnatal Development through α4/β2/α5 Nicotinic Acetylcholine Receptors. Neuropsychopharmacology 2010, 35: 2324-2338. PMID: 20736992, PMCID: PMC2955839, DOI: 10.1038/npp.2010.130.Peer-Reviewed Original ResearchConceptsDevelopmental nicotine exposureNicotine exposureNicotinic acetylcholine receptorsAcetylcholine receptorsΑ5 nicotinic acetylcholine receptorConstituents of smokeEarly post-natal periodPrimary addictive componentΑ5 nAChR subunitTobacco smoke exposureCortico-thalamic connectivityPost-natal periodEarly postnatal developmentPassive avoidance behaviorCorticothalamic neuronsAddictive componentCorticothalamic projectionsSmoke exposureReceptor subtypesNAChR subtypesDevelopmental exposureMouse modelNeurodevelopmental periodAnimal modelsBehavioral alterations
2007
Deficiency in Inhibitory Cortical Interneurons Associates with Hyperactivity in Fibroblast Growth Factor Receptor 1 Mutant Mice
Smith K, Fagel DM, Stevens HE, Rabenstein RL, Maragnoli ME, Ohkubo Y, Picciotto MR, Schwartz ML, Vaccarino FM. Deficiency in Inhibitory Cortical Interneurons Associates with Hyperactivity in Fibroblast Growth Factor Receptor 1 Mutant Mice. Biological Psychiatry 2007, 63: 953-962. PMID: 17988653, DOI: 10.1016/j.biopsych.2007.09.020.Peer-Reviewed Original ResearchMeSH KeywordsAmphetamineAnimalsBehavior, AnimalBiogenic MonoaminesCell CountCentral Nervous System StimulantsCerebral CortexDisease Models, AnimalDopamine AgentsExploratory BehaviorFibroblast Growth Factor 1Glutamate DecarboxylaseHyperkinesisLocomotionMaleMethylphenidateMiceMice, KnockoutMotor ActivityNerve Tissue ProteinsNeural InhibitionNeuronsSignal TransductionConceptsInhibitory cortical circuitsCortical pyramidal neuronsD2 receptor antagonistGrowth factor receptor 1Spontaneous locomotor hyperactivityFibroblast growth factor receptor 1Factor receptor 1Inhibitory neuronal subtypesLocomotor hyperactivityDopamine agonistsCerebral cortexPyramidal neuronsBasal gangliaMotor hyperactivityReceptor antagonistInhibitory interneuronsTyrosine hydroxylaseCortical circuitsPsychiatric disordersLocomotor responseNeuronal subtypesReceptor 1Mutant miceDopamine transporterSpatial learningNicotine‐induced phosphorylation of ERK in mouse primary cortical neurons: evidence for involvement of glutamatergic signaling and CaMKII
Steiner RC, Heath CJ, Picciotto MR. Nicotine‐induced phosphorylation of ERK in mouse primary cortical neurons: evidence for involvement of glutamatergic signaling and CaMKII. Journal Of Neurochemistry 2007, 103: 666-678. PMID: 17666046, DOI: 10.1111/j.1471-4159.2007.04799.x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternCalcium-Calmodulin-Dependent Protein Kinase Type 2Cells, CulturedCerebral CortexCulture MediaDose-Response Relationship, DrugExtracellular Signal-Regulated MAP KinasesFemaleGlutamic AcidIndicators and ReagentsMiceMice, Inbred C57BLMice, KnockoutNeuronsNicotineNicotinic AgonistsPhosphorylationPregnancyReceptors, GlutamateReceptors, NicotinicReverse Transcriptase Polymerase Chain ReactionSignal TransductionSynaptic TransmissionConceptsNicotine-induced ERK phosphorylationExtracellular signal-regulated kinaseERK phosphorylationCAMP-dependent protein kinaseCalmodulin-dependent protein kinase IICalcium/calmodulin-dependent protein kinase IINicotinic acetylcholine receptor inhibitorNicotine-induced phosphorylationSignal-regulated kinaseCortical neuronsProtein kinase IIProtein kinase CMouse primary cortical neuronsKinase II activityAlpha3/beta4Calmodulin-dependent protein kinase II activityGlutamatergic signalingProtein kinaseVoltage-gated sodium channelsKinase IICultured mouse cortical neuronsKinase CCalcium/calmodulin-dependent protein kinase II activityPhosphorylationL-type voltage-gated calcium channels
2006
Human Tobacco Smokers in Early Abstinence Have Higher Levels of β2* Nicotinic Acetylcholine Receptors than Nonsmokers
Staley JK, Krishnan-Sarin S, Cosgrove KP, Krantzler E, Frohlich E, Perry E, Dubin JA, Estok K, Brenner E, Baldwin RM, Tamagnan GD, Seibyl JP, Jatlow P, Picciotto MR, London ED, O'Malley S, van Dyck CH. Human Tobacco Smokers in Early Abstinence Have Higher Levels of β2* Nicotinic Acetylcholine Receptors than Nonsmokers. Journal Of Neuroscience 2006, 26: 8707-8714. PMID: 16928859, PMCID: PMC6674379, DOI: 10.1523/jneurosci.0546-06.2006.Peer-Reviewed Original ResearchConceptsNAChR availabilityNicotinic acetylcholine receptorsEarly abstinenceAbstinent smokersHuman smokersAcetylcholine receptorsExpired carbon monoxide levelsAbility of smokersHuman tobacco smokersProperties of nicotineSingle photon emissionIA-85380Agonist radiotracerUrinary cotinineTobacco smokingTobacco smokersCerebral cortexLast cigaretteNicotine withdrawalWithdrawal symptomsPrevalent subtypeTobacco smokeAddictive chemicalNicotine dependenceSmokers
2003
Neuroprotection by Nicotine in Mouse Primary Cortical Cultures Involves Activation of Calcineurin and L-Type Calcium Channel Inactivation
Stevens TR, Krueger SR, Fitzsimonds RM, Picciotto MR. Neuroprotection by Nicotine in Mouse Primary Cortical Cultures Involves Activation of Calcineurin and L-Type Calcium Channel Inactivation. Journal Of Neuroscience 2003, 23: 10093-10099. PMID: 14602824, PMCID: PMC6740855, DOI: 10.1523/jneurosci.23-31-10093.2003.Peer-Reviewed Original ResearchMeSH KeywordsAlpha7 Nicotinic Acetylcholine ReceptorAnimalsBungarotoxinsCalcineurinCalcineurin InhibitorsCalcium Channel BlockersCalcium Channels, L-TypeCells, CulturedCerebral CortexGlutamic AcidMiceMice, KnockoutNeuronsNeuroprotective AgentsNeurotoxinsNicotineNifedipineReceptors, NicotinicTacrolimusConceptsPrimary cortical culturesL-type channelsNicotine-mediated neuroprotectionCortical culturesNicotine pretreatmentIntracellular calciumCalcium influxActivation of calcineurinBeta2 subunitAlpha7-containing nAChRsL-type calcium channelsEffects of nicotineAbility of nicotineMouse primary cortical culturesNicotinic acetylcholine receptorsCalcium channel inactivationGlutamate excitotoxicityNeuroprotective effectsRole of calciumCalcineurin antagonistsCortical neuronsNeuronal excitabilityGlutamate applicationNeuroprotectionCalcium channelsConditional 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
2002
Decreased Synaptic Vesicle Recycling Efficiency and Cognitive Deficits in Amphiphysin 1 Knockout Mice
Di Paolo G, Sankaranarayanan S, Wenk MR, Daniell L, Perucco E, Caldarone BJ, Flavell R, Picciotto MR, Ryan TA, Cremona O, De Camilli P. Decreased Synaptic Vesicle Recycling Efficiency and Cognitive Deficits in Amphiphysin 1 Knockout Mice. Neuron 2002, 33: 789-804. PMID: 11879655, DOI: 10.1016/s0896-6273(02)00601-3.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCerebral CortexClathrinConditioning, ClassicalEndocytosisFluorescent DyesGABA AntagonistsGlutamic AcidHumansMaze LearningMiceMice, KnockoutNerve Tissue ProteinsNeuronsPentylenetetrazoleProtein IsoformsPyridinium CompoundsQuaternary Ammonium CompoundsSurvival RateSynaptic Vesicles