Administration of a single dose of the recreationally used
drug 3,4-methylenedioxyethamphetamine (
MDEA or "eve") to Dark Agouti rats resulted in an acute dose-dependent hyperthermic response. The peak effect and duration of
hyperthermia 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 (approximately 50%) loss of
5-HT and its metabolite
5-HIAA in cortex, hippocampus and striatum and a similar loss of [3H]-
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), even 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 striatal
dopamine content 7 days later.
MDEA appeared to have about half the potency of
MDMA in inducing acute
hyperthermia and 25% of the potency in inducing degeneration of cerebral
5-HT neurones. However since higher doses of
MDEA (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.