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 differencesFACS Identifies Unique Cocaine-Induced Gene Regulation in Selectively Activated Adult Striatal Neurons
Guez-Barber D, Fanous S, Golden SA, Schrama R, Koya E, Stern AL, Bossert JM, Harvey BK, Picciotto MR, Hope BT. FACS Identifies Unique Cocaine-Induced Gene Regulation in Selectively Activated Adult Striatal Neurons. Journal Of Neuroscience 2011, 31: 4251-4259. PMID: 21411666, PMCID: PMC3073079, DOI: 10.1523/jneurosci.6195-10.2011.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsCocaineCorpus StriatumFemaleFlow CytometryGene ExpressionGene Expression RegulationGenes, Immediate-EarlyImmunohistochemistryNeuronsRatsRats, Sprague-DawleyRats, TransgenicReverse Transcriptase Polymerase Chain ReactionConceptsStriatal neuronsFluorescence-activated cell sortingNeural activity marker FosCocaine-induced locomotionActivity marker FosAdult striatal neuronsUnique gene expression profileP38 MAPK signalingCell-type specificityGene expression profilesSmall proportionTransgenic ratsActivated neuronsImmediate early genesMolecular neuroadaptationsSpecific neuronsGene regulationBehavioral effectsNeuronsAbused drugsMAPK signalingExpression profilesProtein productsCocaineLacZ gene
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
2006
Galanin and galanin‐like peptide modulate neurite outgrowth via protein kinase C‐mediated activation of extracellular signal‐related kinase
Hawes JJ, Narasimhaiah R, Picciotto MR. Galanin and galanin‐like peptide modulate neurite outgrowth via protein kinase C‐mediated activation of extracellular signal‐related kinase. European Journal Of Neuroscience 2006, 23: 2937-2946. PMID: 16819983, DOI: 10.1111/j.1460-9568.2006.04828.x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternCell DifferentiationCells, CulturedDose-Response Relationship, DrugDrug InteractionsEmbryo, MammalianEnzyme ActivationEnzyme InhibitorsExtracellular Signal-Regulated MAP KinasesGalaninGalanin-Like PeptideNeuritesNeuronsProtein Kinase CRatsReceptors, GalaninReverse Transcriptase Polymerase Chain ReactionRNA, MessengerStem CellsConceptsGalanin-like peptideProtein kinase CNervous systemNeurite outgrowthAdult hippocampal progenitor cellsAbility of galaninKinase CERK phosphorylationHippocampal progenitor cellsNeuronal cell line PC12Central nervous systemModulates Neurite OutgrowthExtracellular signal-related kinase (ERK) phosphorylationConcentration-dependent mannerNerve injuryNeuropeptide galaninNeurotrophic effectsExtracellular signal-related kinaseReceptor subtypesNovel physiological roleAdult brainGalaninCell line PC12Signal-related kinaseProgenitor cells