Pharmacology
January 1, 2001
Elisabeth Ratzenboeck, Alois Saria, Norbert Kriechbaum et al.
97 citations
MDMA (ecstasy) is a common illegal drug among European adolescents who are typically inexperienced with hard drugs like cocaine. In rats, the reinforcing effect of intravenously self-administered MDMA did not differ between drug-naive animals and those previously trained with cocaine. MDMA sensitized rats to its own rate-increasing effect but not to that of cocaine. No carryover of cocaine's reinforcing effect to MDMA was observed, indicating that MDMA and cocaine produce distinct interoceptive stimuli in rats.
European Journal of Neuroscience
April 1, 2000
H. S. Fischer, Gerald Zernig, Dieter S. Schatz et al.
54 citations
MDMA (ecstasy) increases the release of the neurotransmitter acetylcholine in rat striatal brain slices in a dose-dependent manner, with a half-maximal effect at about 30 µM. This effect requires calcium and is blocked by tetrodotoxin, indicating it depends on neuronal firing. Blocking glutamate, dopamine D2, serotonin 5-HT1, 5-HT2, 5-HT3C, or muscarinic acetylcholine receptors did not alter MDMA's effect, but blocking histamine H1 receptors completely abolished the acetylcholine release. The findings suggest MDMA directly activates histamine H1 receptors to stimulate striatal cholinergic neurons, revealing a previously unknown neurochemical pathway for MDMA's acute effects.
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.