Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9018293 | Toxicology and Applied Pharmacology | 2005 | 12 Pages |
Abstract
From these findings, it can be postulated that, in our model, METH induces DA release from synaptic vesicles to the cytosol. Simultaneously, METH activates α7 nicotinic receptors, probably inducing depolarization and an increase in intrasynaptosomal Ca2+. This would lead to DAT inhibition and NOS and PKC activation, initiating oxidation of cytosolic DA.
Keywords
DATMDMANBQX1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo[f]quinoxaline-7-sulfonamideaMPTnNOS7-NIMLADCFH-DAEGTADcfDBEα-methyl-p-tyrosine5-HT2′,7′-dichlorofluorescein2′,7′-dichlorofluorescin diacetate7-nitroindazolemethylenedioxymethamphetamineethylene glycol-bis(2-aminoethylether)-N,N,N′,N′-tetraacetic acidDopamine transporterDopaminedihydro-β-erythroidineSerotoninneuronal nitric oxide synthaseMETHMethamphetaminemethyllycaconitine
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Authors
David Pubill, Carlos Chipana, Antonio Camins, Mercè Pallà s, Jordi Camarasa, Elena Escubedo,