2007
Deficiency in Inhibitory Cortical Interneurons Associates with Hyperactivity in Fibroblast Growth Factor Receptor 1 Mutant Mice
Smith K, Fagel DM, Stevens HE, Rabenstein RL, Maragnoli ME, Ohkubo Y, Picciotto MR, Schwartz ML, Vaccarino FM. Deficiency in Inhibitory Cortical Interneurons Associates with Hyperactivity in Fibroblast Growth Factor Receptor 1 Mutant Mice. Biological Psychiatry 2007, 63: 953-962. PMID: 17988653, DOI: 10.1016/j.biopsych.2007.09.020.Peer-Reviewed Original ResearchMeSH KeywordsAmphetamineAnimalsBehavior, AnimalBiogenic MonoaminesCell CountCentral Nervous System StimulantsCerebral CortexDisease Models, AnimalDopamine AgentsExploratory BehaviorFibroblast Growth Factor 1Glutamate DecarboxylaseHyperkinesisLocomotionMaleMethylphenidateMiceMice, KnockoutMotor ActivityNerve Tissue ProteinsNeural InhibitionNeuronsSignal TransductionConceptsInhibitory cortical circuitsCortical pyramidal neuronsD2 receptor antagonistGrowth factor receptor 1Spontaneous locomotor hyperactivityFibroblast growth factor receptor 1Factor receptor 1Inhibitory neuronal subtypesLocomotor hyperactivityDopamine agonistsCerebral cortexPyramidal neuronsBasal gangliaMotor hyperactivityReceptor antagonistInhibitory interneuronsTyrosine hydroxylaseCortical circuitsPsychiatric disordersLocomotor responseNeuronal subtypesReceptor 1Mutant miceDopamine transporterSpatial learning
2006
Human Tobacco Smokers in Early Abstinence Have Higher Levels of β2* Nicotinic Acetylcholine Receptors than Nonsmokers
Staley JK, Krishnan-Sarin S, Cosgrove KP, Krantzler E, Frohlich E, Perry E, Dubin JA, Estok K, Brenner E, Baldwin RM, Tamagnan GD, Seibyl JP, Jatlow P, Picciotto MR, London ED, O'Malley S, van Dyck CH. Human Tobacco Smokers in Early Abstinence Have Higher Levels of β2* Nicotinic Acetylcholine Receptors than Nonsmokers. Journal Of Neuroscience 2006, 26: 8707-8714. PMID: 16928859, PMCID: PMC6674379, DOI: 10.1523/jneurosci.0546-06.2006.Peer-Reviewed Original ResearchConceptsNAChR availabilityNicotinic acetylcholine receptorsEarly abstinenceAbstinent smokersHuman smokersAcetylcholine receptorsExpired carbon monoxide levelsAbility of smokersHuman tobacco smokersProperties of nicotineSingle photon emissionIA-85380Agonist radiotracerUrinary cotinineTobacco smokingTobacco smokersCerebral cortexLast cigaretteNicotine withdrawalWithdrawal symptomsPrevalent subtypeTobacco smokeAddictive chemicalNicotine dependenceSmokers
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
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