Differential effects of intravenous R,S‐(±)‐3,4‐methylenedioxymethamphetamine (MDMA, Ecstasy) and its S(+)‐ and R(−)‐enantiomers on dopamine transmission and extracellular signal regulated kinase phosphorylation (pERK) in the rat nucleus accumbens shell and core
Journal of Neurochemistry January 22, 2007 Elio Acquas, Augusta Pisanu, Saturnino Spiga et al. 52 citations
The stimulant drug MDMA (Ecstasy) increases dopamine transmission in the nucleus accumbens, a brain region involved in reward. This study in male rats examined how the two mirror-image forms (enantiomers) of MDMA—S(+)-MDMA and R(−)-MDMA—affect dopamine release and a downstream signaling molecule called phosphorylated ERK (pERK) in the shell and core of the nucleus accumbens. Racemic MDMA (the standard mixture) and S(+)-MDMA increased dopamine and pERK levels in a dose-related way, with S(+)-MDMA being more potent. R(−)-MDMA had no effect. Blocking D1 dopamine receptors prevented the pERK increase, while blocking D2/D3 receptors did not. The results indicate that the S(+) enantiomer drives MDMA's dopamine-stimulating effects, and pERK serves as a marker of D1-receptor-mediated dopamine signaling.