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
2006
Galanin attenuates cyclic AMP regulatory element‐binding protein (CREB) phosphorylation induced by chronic morphine and naloxone challenge in Cath.a cells and primary striatal cultures
Hawes JJ, Narasimhaiah R, Picciotto MR. Galanin attenuates cyclic AMP regulatory element‐binding protein (CREB) phosphorylation induced by chronic morphine and naloxone challenge in Cath.a cells and primary striatal cultures. Journal Of Neurochemistry 2006, 96: 1160-1168. PMID: 16417577, DOI: 10.1111/j.1471-4159.2005.03613.x.Peer-Reviewed Original ResearchConceptsOpiate withdrawalAdditional potential therapeutic targetsChronic opiate administrationPotential therapeutic targetPrimary striatal culturesExtracellular signal-regulated kinase 1/2 phosphorylationElement-Binding Protein PhosphorylationCAMP regulatory element-binding proteinKinase 1/2 phosphorylationGalanin treatmentMorphine administrationChronic morphineGalanin receptorsNeuropeptide galaninOpiate administrationNaloxone challengeStriatal neuronsLocus coeruleusSomatic signsNucleus accumbensStriatal culturesRegulatory element-binding proteinTherapeutic targetElement-binding proteinMolecular alterations
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
2000
Nicotinic-agonist stimulated 86Rb+ efflux and [3H]epibatidine binding of mice differing in β2 genotype
Marks M, Stitzel J, Grady S, Picciotto M, Changeux J, Collins A. Nicotinic-agonist stimulated 86Rb+ efflux and [3H]epibatidine binding of mice differing in β2 genotype. Neuropharmacology 2000, 39: 2632-2645. PMID: 11044733, DOI: 10.1016/s0028-3908(00)00115-5.Peer-Reviewed Original ResearchConceptsBrain regionsNicotinic acetylcholine receptor functionBeta2 subunitBeta2-containing receptorsAcetylcholine receptor functionHigh-affinity siteBeta2 subunit expressionBinding of mouseCerebral cortexNicotinic responsesMicroM nicotineOlfactory bulbInferior colliculusNicotinic agonistsSubunit expressionReceptor functionLow affinityLow affinity sitesDHbetaEInhibitionMiceStimulationEffluxCytisineNull mutation