2012
Naltrexone does not attenuate the effects of intravenous Δ9-tetrahydrocannabinol in healthy humans
Ranganathan M, Carbuto M, Braley G, Elander J, Perry E, Pittman B, Radhakrishnan R, Sewell RA, D'Souza DC. Naltrexone does not attenuate the effects of intravenous Δ9-tetrahydrocannabinol in healthy humans. The International Journal Of Neuropsychopharmacology 2012, 15: 1251-1264. PMID: 22243563, DOI: 10.1017/s1461145711001830.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAttentionBehaviorCognitionCognition DisordersDouble-Blind MethodDronabinolDrug InteractionsEuphoriaFemaleHallucinogensHumansInhibition, PsychologicalInjections, IntravenousMaleMarijuana AbuseMemoryMental RecallMiddle AgedNaltrexoneNarcotic AntagonistsOrientationPerceptionPsychoses, Substance-InducedRecognition, PsychologyRewardYoung AdultConceptsCognitive effectsHealthy human subjectsPerceptual alterationsHuman subjectsTHC effectsCognitive impairmentΔ9-tetrahydrocannabinolActive naltrexoneDouble-blind mannerTest dayPsychotomimetic effectsPreclinical evidenceMOR antagonistΜ-opioidCB1R agonistPsychiatric illnessPrecise natureHealthy humansDrug AdministrationReceptor systemNaltrexoneEffect of pretreatmentAnxietyPlaceboTHC
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
1999
Genetic alteration of phospholipase C β3 expression modulates behavioral and cellular responses to μ opioids
Xie W, Samoriski G, McLaughlin J, Romoser V, Smrcka A, Hinkle P, Bidlack J, Gross R, Jiang H, Wu D. Genetic alteration of phospholipase C β3 expression modulates behavioral and cellular responses to μ opioids. Proceedings Of The National Academy Of Sciences Of The United States Of America 1999, 96: 10385-10390. PMID: 10468617, PMCID: PMC17897, DOI: 10.1073/pnas.96.18.10385.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBrainCalcium ChannelsCell MembraneEnkephalin, Ala(2)-MePhe(4)-Gly(5)-EnkephalinsGanglia, SpinalGene Expression RegulationGene Expression Regulation, EnzymologicIsoenzymesMembrane PotentialsMiceMice, KnockoutMorphineNeurons, AfferentPainPhospholipase C betaReceptors, Opioid, deltaReceptors, Opioid, kappaReceptors, Opioid, muType C PhospholipasesConceptsBeta3-null miceDorsal root ganglion neuronsPLC-beta3Mu-opioid responseOpioid receptor numberSpecific mu agonistPrimary sensory neuronsPhospholipase CDelta-opioid receptorsWild-type neuronsBeta3-deficient miceProtein kinase CDAMGO responseMicro opioidsOpioid responseOpioid regulationMu agonistsOpioid sensitivityGanglion neuronsΜ-opioidOpioid receptorsReceptor numberSensory neuronsKinase CNumber of intracellular
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