Researchers investigated the potential anti-Parkinson’s disease effects of racemic MDMA, R-(-)-MDMA, S-(+)-MDMA and related drugs (MDE (racemic, R-(-) and S-(+) enantiomers), MDA and MBDB) via a rat model of Parkinson’s disease. The researchers induced catalepsy via 0.5 mg/kg injection of haloperidol (dopamine D2 antagonist). Catalepsy was measured by measuring descent latency, or how long it took rats to remove their paws from an elevated horizontal bar and a vertical grid from 60 minutes after haloperidol administration onward. Haloperidol was administered along with saline, racemic MDMA (1, 2.5 or 5 mg/kg), 2.5 mg/kg R-(-)-MDMA, 2.5 mg/kg S-(+)-MDMA, 2.5 or 5 mg/kg MDE, MDA, MBDB, 5 mg/kg R-(-)-MDE or 5 mg/kg S-(-)-MDE. All doses of racemic MDMA reduced descent latency (rats moved their paws more rapidly), and higher doses of MDMA produced greater reductions in descent latency. S-(+)-MDMA reduced descent latency, though not to the same degree as racemic MDMA, and R-(-)-MDMA failed to reduce descent latency. Racemic MDE was less potent than MDMA in reducing descent latency, though it did reduce descent latency, with the higher dose more effective than the lower dose. Both R-(-)-MDE and S-(+)-MDE had lesser anti-cataleptic effects than racemic MDE, but R-(-)-MDE had a greater impact on descent latency than S-(-)-MDE. Racemic MDA and MBDB both had similarly negligible effects on descent latency. The researchers considered several explanations for the anti-cataleptic effects of these drugs. Serotonin release appears not to be involved, as all drugs tested release similar amounts of serotonin, and dopamine release may play a role, but if so, then it is puzzling that MDA is not as good at reducing descent latency as MDE, since MDA is a more potent dopamine releaser than MDE (Nichols and Oberlender 1990). The authors conclude that 5HT₂ receptor agonism may play a role in the anti-cataleptic action of MDMA and related drugs. It should be pointed out that MDA, MDMA and MDE were all administered at the same dose, despite evidence that MDA is more potent than MDMA, and MDE less potent (Shulgin and Nichols 1978; Nichols and Oberlender 1986), so it is possible that some differences in effect may relate to differences in potency. Taken together, study findings suggest that entactogens may possess anti-Parkinson’s disease effects, and that further study may lead to the development of novel pharmacological treatments for Parkinson’s disease. This is also the first of three reports by the same team (see also Banjaw et al. 2003; Lebsanft et al. 2003). Note that a study using rotation direction in rats with one-sided (unilateral) lesions of dopamine neurons found that MDA was most potent at inducing rotation in the direction of the lesion, considered a sign of anti-Parkinson’s disease effects or of capacity to counter side effects of other anti-Parkinson’s medications. This raises issues concerning possible differences in pharmacological actions involved in the two rodent models of Parkinson’s disease studied by this team.