The acute effect in rats of 3,4-methylenedioxyethamphetamine (MDEA,"eve") on body temperature and long term degeneration of 5-HT neurones in brain: Acomparison with MDMA ("ecstasy")

Administration of a single dose of the recreationally used drug 3,4-methyle nedioxyethamphetamine (MDEA or "eve") to Dark Agouti rats resulted in an ac ute dose-dependent hyperthermic response. The peak effect and duration of h yperthermia of a dose of MDEA of 35 mg/kg intraperitoneally was similar to a dose of 3,4-methylenedioxymethamphetamine (MDMA or "ecstasy") of 15 mg/kg intraperitoneally. Seven days later this dose of MDMA produced a marked (a pproximate to 50%) loss of 5-HT and its metabolite 5-HIAA in cortex, hippoc ampus and striatum and a similar loss of [H-3]-paroxetine binding in cortex ; these losses reflecting the MDMA-induced neurotoxic degeneration of 5-HT nerve endings. In contrast, administration of MDEA (15, 25 or 35 mg/kg), ev en at the highest dose, produced only a 20% loss in cortex and hippocampus and no decrease in striatum. The neurotoxic effect of MDEA was only weakly dose-dependent. Neither MDEA (35 mg/kg) nor MDMA (15 mg/kg) altered striata l dopamine content 7 days later. MDEA appeared to have about half the poten cy of MDMA in inducing acute hyperthermia and 25% of the potency in inducin g degeneration of cerebral 5-HT neurones. However since higher doses of MDE A (compared to MDMA) are probably necessary to induce mood changing effects , these data do not support any contention that this compound is a "safer" recreational drug than MDMA in terms of either acute toxicity or long term neurodegeneration.