6533b7d8fe1ef96bd126a2aa

RESEARCH PRODUCT

Sensitivity of neuronal nicotinic acetylcholine receptors to the opiate antagonists naltrexone and naloxone: receptor blockade and up-regulation

Luis E.f. AlmeidaAlfred MaelickeEdson X. AlbuquerqueEdson X. AlbuquerqueAdriana L CamaraAdriana L CamaraEdna F. R. Pereira

subject

NicotinePatch-Clamp TechniquesTime FactorsNarcotic AntagonistsClinical BiochemistryGene ExpressionPharmaceutical Science(+)-NaloxoneReceptors NicotinicPharmacologyHippocampal formationSensitivity and Specificitycomplex mixturesBiochemistryNaltrexoneCell LineNicotineStructure-Activity Relationshipmental disordersDrug DiscoverymedicineHumansMolecular BiologyAcetylcholine receptorNeuronsNaloxoneChemistryNarcotic antagonistmusculoskeletal neural and ocular physiologyOrganic ChemistryNaltrexoneUp-RegulationNicotinic agonistnervous systemMechanism of actionMolecular MedicineSmoking Cessationsense organsmedicine.symptommedicine.drug

description

In HEK293 cells stably expressing alpha4beta2 nAChRs, naltrexone, but not naloxone, blocked alpha4beta2 nAChRs via an open-channel blocking mechanism. In primary hippocampal cultures, naltrexone inhibited alpha7 nAChRs up-regulated by nicotine, and in organotypic hippocampal cultures naltrexone caused a time-dependent up-regulation of functional alpha7 nAChRs that was detected after removal of the drug. These results indicate that naltrexone could be used as a smoking cessation aid.

yearjournalcountryeditionlanguage
2003-11-17Bioorganic & Medicinal Chemistry Letters
https://doi.org/10.1016/j.bmcl.2004.01.004