2019
Nicotinic Acetylcholine Receptor Signaling in the Hypothalamus: Mechanisms Related to Nicotine’s Effects on Food Intake
Calarco CA, Picciotto MR. Nicotinic Acetylcholine Receptor Signaling in the Hypothalamus: Mechanisms Related to Nicotine’s Effects on Food Intake. Nicotine & Tobacco Research 2019, 22: 152-163. PMID: 30690485, PMCID: PMC7297099, DOI: 10.1093/ntr/ntz010.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsFood intakeNicotinic acetylcholine receptorsWeight gainBody weightPreclinical workAcetylcholine receptorsPost-cessation weight gainOrexigenic agouti-related peptideAnorexigenic proopiomelanocortin (POMC) neuronsNicotine replacement therapyAgouti-related peptideNicotinic agonist cytisineAbility of nicotineLower body weightProopiomelanocortin neuronsNicotine administrationHypothalamic circuitsReplacement therapyArcuate nucleusNicotine effectsNicotine actsAgonist cytisineAverage weight gainTobacco useRodent models
2012
Nicotinic Regulation of Energy Homeostasis
Zoli M, Picciotto MR. Nicotinic Regulation of Energy Homeostasis. Nicotine & Tobacco Research 2012, 14: 1270-1290. PMID: 22990212, PMCID: PMC3611985, DOI: 10.1093/ntr/nts159.Peer-Reviewed Original ResearchConceptsEnergy homeostasisCellular targetsPossible molecular targetsPrimary psychoactive substanceCell typesNicotinic acetylcholine receptor subtypesEnergy metabolismAcetylcholine receptor subtypesAbility of nicotineEffects of nicotineRegulation of feedingMolecular targetsFunctional featuresRegulationNicotinic regulationHomeostasisReceptor subtypesNAChR subtypesTobacco smokeBody weightNeuroendocrine systemRecent studiesNicotineMetabolismMammals
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
Neuroprotection via nAChRs: the role of nAChRs in neurodegenerative disorders such as Alzheimer's and Parkinson's disease.
Picciotto MR, Zoli M. Neuroprotection via nAChRs: the role of nAChRs in neurodegenerative disorders such as Alzheimer's and Parkinson's disease. Frontiers In Bioscience-Landmark 2008, 13: 492-504. PMID: 17981563, DOI: 10.2741/2695.Peer-Reviewed Original ResearchConceptsAbility of nicotineNeurodegenerative disordersRole of nAChRsHuman neurodegenerationNeuroprotective agentsParkinson's diseaseDevelopmental stagesCellular effectsNicotine-mediated neuroprotectionRegimen of administrationDrug discoveryNicotine neuroprotectionNeuronal survivalNeuronal deathEpidemiological studiesNicotinic compoundsAlzheimer's diseaseRecent studiesNeuroprotectionDiseaseNicotineCompelling evidenceNAChRsVivoFull understanding
2007
Genetics of nicotinic acetylcholine receptors: Relevance to nicotine addiction
Mineur YS, Picciotto MR. Genetics of nicotinic acetylcholine receptors: Relevance to nicotine addiction. Biochemical Pharmacology 2007, 75: 323-333. PMID: 17632086, PMCID: PMC2212607, DOI: 10.1016/j.bcp.2007.06.010.Peer-Reviewed Original ResearchConceptsGene productsNicotinic acetylcholine receptorsClassical genetic approachesClasses of genesNicotine dependenceGenetic engineering studiesNumber of genesGenetic engineering techniquesNicotine addictionAnimal studiesAcetylcholine receptorsGene association studiesHuman twin studiesNumber of subunitsSubstantial genetic componentGenetic approachesGenetic basisDopaminergic cell bodiesAbility of nicotineVentral tegmental areaAssociation studiesLines of evidenceGenetic componentNicotine-related behaviorsMesolimbic system
2006
Nicotine withdrawal increases body weight, neuropeptide Y and Agouti-related protein expression in the hypothalamus and decreases uncoupling protein-3 expression in the brown adipose tissue in high-fat fed mice
Fornari A, Pedrazzi P, Lippi G, Picciotto MR, Zoli M, Zini I. Nicotine withdrawal increases body weight, neuropeptide Y and Agouti-related protein expression in the hypothalamus and decreases uncoupling protein-3 expression in the brown adipose tissue in high-fat fed mice. Neuroscience Letters 2006, 411: 72-76. PMID: 17052838, DOI: 10.1016/j.neulet.2006.10.014.Peer-Reviewed Original ResearchMeSH KeywordsAdipose Tissue, BrownAgouti Signaling ProteinAgouti-Related ProteinAnalysis of VarianceAnimalsBody WeightDietary FatsHypothalamusIntercellular Signaling Peptides and ProteinsIon ChannelsMaleMiceMice, Inbred C57BLMitochondrial ProteinsNeuropeptide YNicotineNicotinic AgonistsReceptors, Adrenergic, betaSubstance Withdrawal SyndromeUncoupling Protein 3ConceptsNicotine withdrawalBrown adipose tissueBody weightNeuropeptide YAdipose tissueOrexigenic peptides neuropeptide YHigh-fat fed miceChronic nicotine treatmentPeptides neuropeptide YHigh-fat dietAbility of nicotineBody weight regulationProtein 3 expressionAnorectic effectNicotine treatmentSmoking cessationFat dietFed miceHuman smokersNormal rodentsWeight regulationIncreased expressionProtein 3Protein expressionExposure results
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 channels