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 ResearchMeSH KeywordsAnimalsBrainCognitionHumansMental DisordersNicotineProtein TransportReceptors, NicotinicRewardSynaptic TransmissionUp-RegulationConceptsPsychiatric 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
2011
Striatal‐enriched protein tyrosine phosphatase (STEP) knockout mice have enhanced hippocampal memory
Venkitaramani DV, Moura PJ, Picciotto MR, Lombroso PJ. Striatal‐enriched protein tyrosine phosphatase (STEP) knockout mice have enhanced hippocampal memory. European Journal Of Neuroscience 2011, 33: 2288-2298. PMID: 21501258, PMCID: PMC3118976, DOI: 10.1111/j.1460-9568.2011.07687.x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBehavior, AnimalFocal Adhesion Kinase 2HippocampusMemoryMiceMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PhosphorylationProtein Tyrosine Phosphatases, Non-ReceptorReceptors, AMPAReceptors, N-Methyl-D-AspartateSynaptic TransmissionConceptsStriatal-enriched protein tyrosine phosphataseSTEP KO miceProtein tyrosine phosphataseBrain-specific phosphataseProline-rich tyrosine kinaseEffect of deletionN-methyl-D-aspartate receptorsERK1/2 substratesNR1/NR2B N‐Methyl‐d‐Aspartate ReceptorsPotential molecular mechanismsTyrosine phosphataseSignaling proteinsTyrosine phosphorylationDownstream effectorsKinase 1/2Molecular mechanismsTyrosine kinaseFunctional importanceKnockout micePhosphorylationSTEP knockout miceSynaptic strengtheningIsoxazole propionic acid (AMPA) receptorsSynaptosomal expressionRegulation
2010
Mice lacking the galanin gene show decreased sensitivity to nicotine conditioned place preference
Neugebauer NM, Henehan RM, Hales CA, Picciotto MR. Mice lacking the galanin gene show decreased sensitivity to nicotine conditioned place preference. Pharmacology Biochemistry And Behavior 2010, 98: 87-93. PMID: 21172385, PMCID: PMC3030658, DOI: 10.1016/j.pbb.2010.12.015.Peer-Reviewed Original ResearchConceptsGal-/- miceAcute nicotine administrationNicotine CPPPlace preferenceNicotine administrationRewarding effectsRole of galaninEffects of nicotineNucleus accumbens shellClass of drugsAmphetamine place preferenceDrugs of abuseGalanin signalingNeuropeptide galaninCPP chamberAlcohol drinkingNicotine rewardSignificant CPPExtracellular signal-related kinaseAccumbens shellGalanin peptideHigh doseSystem activationAlcohol preferenceSignal-related kinase
2009
Nucleus Accumbens CREB Activity is Necessary for Nicotine Conditioned Place Preference
Brunzell DH, Mineur YS, Neve RL, Picciotto MR. Nucleus Accumbens CREB Activity is Necessary for Nicotine Conditioned Place Preference. Neuropsychopharmacology 2009, 34: 1993-2001. PMID: 19212318, PMCID: PMC2709692, DOI: 10.1038/npp.2009.11.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsConditioning, PsychologicalCuesCyclic AMP Response Element-Binding ProteinDecision MakingDose-Response Relationship, DrugDown-RegulationGene Transfer TechniquesMaleMiceMice, Inbred C57BLNicotineNicotinic AgonistsNucleus AccumbensPhosphorylationRewardSynaptic TransmissionTobacco Use DisorderUp-RegulationConceptsCyclic AMP response element binding proteinNAc shellPlace preferenceNicotine CPPCREB activityModulation of cocaineCREB activationNicotine place preferenceAbility of nicotineAbsence of nicotineCue-induced responsesDominant-negative CREB constructNicotinic acetylcholine receptorsAMP response element binding proteinLevels of CREBTranscription factor cyclic AMP response element binding proteinViral-mediated gene transferRange of dosesActivation of intracellularNicotine exposureMorphine rewardC57BL/6J miceNicotine rewardDopamine neuronsLong-term consequences
2008
Regulation of Synaptic Efficacy in Hypocretin/Orexin-Containing Neurons by Melanin Concentrating Hormone in the Lateral Hypothalamus
Rao Y, Lu M, Ge F, Marsh DJ, Qian S, Wang AH, Picciotto MR, Gao XB. Regulation of Synaptic Efficacy in Hypocretin/Orexin-Containing Neurons by Melanin Concentrating Hormone in the Lateral Hypothalamus. Journal Of Neuroscience 2008, 28: 9101-9110. PMID: 18784290, PMCID: PMC2562258, DOI: 10.1523/jneurosci.1766-08.2008.Peer-Reviewed Original ResearchMeSH KeywordsAction PotentialsAnalysis of VarianceAnimalsAnimals, NewbornBehavior, AnimalBenzazepinesBenzhydryl CompoundsCentral Nervous System StimulantsDopamine AgonistsDose-Response Relationship, DrugExcitatory Amino Acid AgentsGlutamic AcidGreen Fluorescent ProteinsHypothalamic Area, LateralHypothalamic HormonesIn Vitro TechniquesIntracellular Signaling Peptides and ProteinsMelaninsMiceMice, Inbred C57BLMice, TransgenicModafinilMotor ActivityNeuronsNeuropeptidesOrexinsPertussis ToxinPituitary HormonesReceptors, SomatostatinSynapsesSynaptic TransmissionTime FactorsConceptsHypocretin/orexin neuronsMCHR1 KO miceOrexin-containing neuronsLateral hypothalamusWild-type miceOrexin neuronsHypocretin/orexinKO miceMCH receptor 1Action potential firingEffects of modafinilMelanin-Concentrating HormoneHypocretin/orexin signalingGroups of neuronsMCH neuronsMiniature EPSCsWT miceHypocretin/Glutamatergic synapsesOrexin signalingSynaptic transmissionPertussis toxinBrain areasReciprocal innervationInhibitory influenceVoluntary oral nicotine intake in mice down-regulates GluR2 but does not modulate depression-like behaviors
Vieyra-Reyes P, Picciotto MR, Mineur YS. Voluntary oral nicotine intake in mice down-regulates GluR2 but does not modulate depression-like behaviors. Neuroscience Letters 2008, 434: 18-22. PMID: 18261852, PMCID: PMC2757003, DOI: 10.1016/j.neulet.2008.01.021.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, OralAnimalsAnxiety DisordersBehavior, AnimalBrainCyclic AMP Response Element-Binding ProteinDepressive DisorderDown-RegulationGlutamic AcidMaleMiceMice, Inbred BALB CMice, Inbred C57BLMotor ActivityNeural PathwaysNicotineNicotinic AgonistsNucleus AccumbensReceptors, AMPARewardSynaptic TransmissionTobacco Use DisorderVentral Tegmental AreaVolitionConceptsCAMP response element-binding proteinDepression-like behaviorVentral tegmental areaNucleus accumbensMesolimbic systemNicotine preferenceChronic nicotine exposureDepression-related behaviorsNon-treated animalsBALB/cOral nicotine intakeCentral nervous systemResponse element-binding proteinNicotine exposureNicotine rewardMesolimbic dopamine projectionsTegmental areaNicotine intakeGlutamate receptorsDopamine projectionsElement-binding proteinNervous systemLocomotor activityMice C57BL/6JGluR1 levels
2007
Nicotine‐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
2003
Identification and Characterization of AplysiaAdducin, an Aplysia Cytoskeletal Protein Homologous to Mammalian Adducins: Increased Phosphorylation at a Protein Kinase C Consensus Site during Long-Term Synaptic Facilitation
Gruenbaum LM, Gilligan DM, Picciotto MR, Marinesco S, Carew TJ. Identification and Characterization of AplysiaAdducin, an Aplysia Cytoskeletal Protein Homologous to Mammalian Adducins: Increased Phosphorylation at a Protein Kinase C Consensus Site during Long-Term Synaptic Facilitation. Journal Of Neuroscience 2003, 23: 2675-2685. PMID: 12684453, PMCID: PMC6742073, DOI: 10.1523/jneurosci.23-07-02675.2003.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsAplysiaCalmodulin-Binding ProteinsCloning, MolecularConsensus SequenceCytoskeletal ProteinsHumansKineticsMammalsMiceModels, BiologicalMolecular Sequence DataMotor NeuronsNervous SystemNeuronal PlasticityNeuronsNeurons, AfferentPhosphorylationProtein Kinase CProtein Structure, TertiarySequence Homology, Amino AcidSerotoninSynaptic TransmissionConceptsMammalian adducinsProtein kinase CProtein kinase C consensus sitesLong-term facilitationPKC phosphorylation sitesAplysia nervous systemProtein HomologousPhosphorylation sitesConsensus sitesMembrane cytoskeletonRegulatory componentsCandidate proteinsLong-term synaptic facilitationKinase CAdducinAplysia homologIncreased phosphorylationPhosphorylationNervous system extractsAplysia neuronsShort-term facilitationParticulate fractionSynaptic alterationsMotor neuronsSynaptic transmission