2019
Role of Neuronal VEGF Signaling in the Prefrontal Cortex in the Rapid Antidepressant Effects of Ketamine
Deyama S, Bang E, Wohleb ES, Li XY, Kato T, Gerhard DM, Dutheil S, Dwyer JM, Taylor SR, Picciotto MR, Duman RS. Role of Neuronal VEGF Signaling in the Prefrontal Cortex in the Rapid Antidepressant Effects of Ketamine. American Journal Of Psychiatry 2019, 176: 388-400. PMID: 30606046, PMCID: PMC6494682, DOI: 10.1176/appi.ajp.2018.17121368.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, NeutralizingBehavior, AnimalExcitatory Amino Acid AntagonistsGene Knockdown TechniquesGene Knockout TechniquesIn Vitro TechniquesKetamineMiceNeuronsPrefrontal CortexQuinazolinesSignal TransductionVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2ConceptsNeuronal vascular endothelial growth factorVascular endothelial growth factorMedial prefrontal cortexRapid antidepressant actionsAntidepressant actionIntra-mPFC infusionSystemic ketamineBehavioral actionsFlk-1Conventional monoamine-based antidepressantsPrefrontal cortexRole of VEGFRapid antidepressant effectsTreatment-resistant depressionMethyl-d-aspartate receptor antagonist ketamineNeuron-specific deletionMonoamine-based antidepressantsNeuron-specific knockoutViral-mediated knockdownEndothelial growth factorVEGF-Flk-1Synaptogenic actionsAntidepressant effectsSynaptogenic effectsLocal knockdown
2015
DARPP-32 interaction with adducin may mediate rapid environmental effects on striatal neurons
Engmann O, Giralt A, Gervasi N, Marion-Poll L, Gasmi L, Filhol O, Picciotto MR, Gilligan D, Greengard P, Nairn AC, Hervé D, Girault JA. DARPP-32 interaction with adducin may mediate rapid environmental effects on striatal neurons. Nature Communications 2015, 6: 10099. PMID: 26639316, PMCID: PMC4675091, DOI: 10.1038/ncomms10099.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBehavior, AnimalBrainCaffeineCalmodulin-Binding ProteinsCentral Nervous System StimulantsChlorocebus aethiopsCocaineCOS CellsDendritic SpinesDopamine and cAMP-Regulated Phosphoprotein 32EnvironmentFluorescence Recovery After PhotobleachingImmunoblottingImmunohistochemistryIn Vitro TechniquesMass SpectrometryMiceMice, Inbred C57BLMutationNeostriatumNeuronsNucleus AccumbensPhosphorylationRatsRats, Sprague-DawleyRewardConceptsAdducin phosphorylationCytoskeletal proteinsActin filamentsMolecular pathwaysCellular mechanismsEnvironmental changesPhosphorylationDARPP-32Striatal neuronsAdducinMutant miceSynaptic stabilityProteinCascadeMultiple effectsEnvironmental effectsBindsDendritic spinesNeuronsModification of responsesBrief exposurePathwayInteractionFilamentsEnrichment
2011
Decreased α4β2 nicotinic receptor number in the absence of mRNA changes suggests post‐transcriptional regulation in the spontaneously hypertensive rat model of ADHD
Wigestrand MB, Mineur YS, Heath CJ, Fonnum F, Picciotto MR, Walaas SI. Decreased α4β2 nicotinic receptor number in the absence of mRNA changes suggests post‐transcriptional regulation in the spontaneously hypertensive rat model of ADHD. Journal Of Neurochemistry 2011, 119: 240-250. PMID: 21824140, PMCID: PMC3171636, DOI: 10.1111/j.1471-4159.2011.07415.x.Peer-Reviewed Original ResearchMeSH KeywordsAconitineAnimalsAttention Deficit Disorder with HyperactivityAzetidinesBrain ChemistryBridged Bicyclo Compounds, HeterocyclicBungarotoxinsIn Vitro TechniquesKineticsMaleMembranesNicotinic AgonistsNicotinic AntagonistsProtein Processing, Post-TranslationalPyridinesRatsRats, Inbred SHRRats, Inbred WKYReceptors, NicotinicReverse Transcriptase Polymerase Chain ReactionRNA, MessengerThermodynamicsConceptsAttention-deficit/hyperactivity disorderQuantitative real-time PCRBrain regionsCerebellum of SHRWistar-Kyoto rat controlsHypertensive rat modelMRNA levelsNicotinic receptor numbersCentral nicotinic receptorsSpecific brain regionsAdditional brain regionsSHR brainHypertensive ratsRat modelReal-time PCRNicotinic receptorsReceptor numberEpidemiological studiesLevels of mRNAΑ4β2 nAChRsSHRWKYNAChRsHyperactivity disorderStrain differences
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 influence
2003
Nicotine Induces Glutamate Release from Thalamocortical Terminals in Prefrontal Cortex
Lambe EK, Picciotto MR, Aghajanian GK. Nicotine Induces Glutamate Release from Thalamocortical Terminals in Prefrontal Cortex. Neuropsychopharmacology 2003, 28: 216-225. PMID: 12589374, DOI: 10.1038/sj.npp.1300032.Peer-Reviewed Original ResearchConceptsPrefrontal cortexSpontaneous excitatory postsynaptic currentsPrefrontal cortical activationEmotional cuesHigh-affinity nicotinic receptorsCognitive functionCortical activationThalamocortical terminalsGlutamate releaseBrain regionsLayer V pyramidal neuronsCognitionPrefrontal cortical slicesExcitatory postsynaptic currentsRelease of glutamateCortexStimulation of nAChRsNicotinic acetylcholine receptorsΑ4β2 nAChRsDifferent neurotransmittersCerebral cortexPyramidal neuronsCortical slicesPostsynaptic currentsΜ-opioid
2000
The Dopamine/D1 Receptor Mediates the Phosphorylation and Inactivation of the Protein Tyrosine Phosphatase STEP via a PKA-Dependent Pathway
Paul S, Snyder G, Yokakura H, Picciotto M, Nairn A, Lombroso P. The Dopamine/D1 Receptor Mediates the Phosphorylation and Inactivation of the Protein Tyrosine Phosphatase STEP via a PKA-Dependent Pathway. Journal Of Neuroscience 2000, 20: 5630-5638. PMID: 10908600, PMCID: PMC6772528, DOI: 10.1523/jneurosci.20-15-05630.2000.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAnimalsCatalytic DomainCorpus StriatumCyclic AMP-Dependent Protein KinasesEnzyme ActivationIn Vitro TechniquesMaleMolecular Sequence DataNeuronsPhosphoproteinsPhosphorus RadioisotopesPhosphorylationProtein Tyrosine PhosphatasesProtein Tyrosine Phosphatases, Non-ReceptorRatsRats, Sprague-DawleyReceptors, Dopamine D1Signal TransductionConceptsProtein tyrosine phosphatase familyCAMP-dependent protein kinaseTryptic phosphopeptide mappingPotential phosphorylation sitesUnique N-terminalProtein-protein interactionsMembrane-associated proteinsRole of phosphorylationTyrosine phosphatase familyAmino acid sequenceSite-directed mutagenesisAmino acid sequencingPKA-dependent pathwayTyrosine phosphatase STEPPhosphatase familyPhosphopeptide mappingPhosphorylation sitesAlternative splicingSubcellular compartmentsProtein kinaseTerminal domainEquivalent residuesCytosolic proteinsSpecific residuesAcid sequence5-Iodo-A-85380, an α4β2 Subtype-Selective Ligand for Nicotinic Acetylcholine Receptors
Mukhin A, Gündisch D, Horti A, Koren A, Tamagnan G, Kimes A, Chambers J, Vaupel D, King S, Picciotto M, Innis R, London E. 5-Iodo-A-85380, an α4β2 Subtype-Selective Ligand for Nicotinic Acetylcholine Receptors. Molecular Pharmacology 2000, 57: 642-649. PMID: 10692507, DOI: 10.1124/mol.57.3.642.Peer-Reviewed Original ResearchConceptsNicotinic acetylcholine receptorsAlpha4beta2 nAChRsAcetylcholine receptorsNeuronal nicotinic acetylcholine receptorsAffinity of epibatidineRat adrenal glandMuscle-type nAChRsSubtype-selective ligandsAlpha4beta2 subtypeAdrenal glandRat brainSelective radioligandBrain regionsNAChRsBeta4 subunitsRadioiodinated ligandBeta2 subunitVivo studiesEpibatidineVivo experimentsHuman brainSubtypesRadioligandBrainReceptors
1999
Two pharmacologically distinct components of nicotinic receptor-mediated rubidium efflux in mouse brain require the beta2 subunit.
Marks MJ, Whiteaker P, Calcaterra J, Stitzel JA, Bullock AE, Grady SR, Picciotto MR, Changeux JP, Collins AC. Two pharmacologically distinct components of nicotinic receptor-mediated rubidium efflux in mouse brain require the beta2 subunit. Journal Of Pharmacology And Experimental Therapeutics 1999, 289: 1090-103. PMID: 10215692.Peer-Reviewed Original ResearchConceptsBeta2 subunitBeta2 null mutant miceConcentration-effect curvesMouse brain synaptosomesAlpha4beta2 receptorsBrain synaptosomesNicotinic agonistsMouse brainRubidium effluxMutant miceLine radioactivity detectionDHbetaEAgonistsEffluxBrainStimulationRadioactivity detectionPotencyHexamethoniumErythroidineResponseAcetylcholineMethyllycaconitineAntagonistBungarotoxin
1998
Acetylcholine receptors containing the β2 subunit are involved in the reinforcing properties of nicotine
Picciotto M, Zoli M, Rimondini R, Léna C, Marubio L, Pich E, Fuxe K, Changeux J. Acetylcholine receptors containing the β2 subunit are involved in the reinforcing properties of nicotine. Nature 1998, 391: 173-177. PMID: 9428762, DOI: 10.1038/34413.Peer-Reviewed Original ResearchMeSH Keywords3,4-Dihydroxyphenylacetic AcidAcetylcholineAnimalsBinding SitesCarrier ProteinsCocaineConditioning, OperantDopamineDopamine Plasma Membrane Transport ProteinsHomovanillic AcidIn Vitro TechniquesMaleMembrane GlycoproteinsMembrane Transport ProteinsMiceMice, Inbred C57BLMice, Inbred DBAMice, KnockoutMicrodialysisMotor ActivityNerve Tissue ProteinsNicotineNucleus AccumbensPatch-Clamp TechniquesReceptors, NicotinicSecond Messenger SystemsSubstantia NigraVentral Tegmental AreaConceptsProperties of nicotineAcetylcholine receptorsVentral striatumΒ2 subunitNeuronal nicotinic acetylcholine receptorsMesencephalic dopaminergic neuronsEffects of nicotineWild-type micePatch-clamp recordingsMesolimbic dopamine systemNicotinic acetylcholine receptorsDrugs of abuseDopaminergic neuronsMesolimbic systemDopamine releaseDopamine systemMutant miceMiceNicotineNeurotransmitter dopamineStriatumReceptorsNeuronsReleaseBrain
1995
The Regulatory Region of Calcium/Calmodulin-dependent Protein Kinase I Contains Closely Associated Autoinhibitory and Calmodulin-binding Domains (∗)
Yokokura H, Picciotto M, Nairn A, Hidaka H. The Regulatory Region of Calcium/Calmodulin-dependent Protein Kinase I Contains Closely Associated Autoinhibitory and Calmodulin-binding Domains (∗). Journal Of Biological Chemistry 1995, 270: 23851-23859. PMID: 7559563, DOI: 10.1074/jbc.270.40.23851.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsBase SequenceBinding SitesCalcium-Calmodulin-Dependent Protein Kinase Type 1Calcium-Calmodulin-Dependent Protein KinasesCalmodulinDNA, ComplementaryEnzyme InhibitorsIn Vitro TechniquesMolecular Sequence DataMutagenesisMyosin-Light-Chain KinaseRatsRecombinant Fusion ProteinsSequence DeletionSequence Homology, Amino AcidStructure-Activity RelationshipConceptsCaM kinase IKinase IProtein kinase ITruncation mutantsCalmodulin-dependent protein kinase ICalcium/calmodulin-dependent protein kinase IDependent protein kinase IDependent protein kinaseSyntide-2Active kinaseAutoinhibitory domainDependent activityGlutathione S-transferaseProtein kinaseRegulatory regionsActive mutantMutantsFusion proteinPeptide substratesIntrasteric mechanismGlutathione-Sepharose 4B.COOH-terminalS-transferase