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The Acute Effect in Rats of 3, 4‐Methylenedioxyethamphetamine (MDEA, “Eve”) on Body Temperature and Long Term Degeneration of 5‐HT Neurones in Brain: A Comparison with MDMA (“Ecstasy”)

María Isabel Colado, Raquel Ena María Granados, Esther O’shea, B. Moreno Esteban, Alfred Richard Green

Pharmacology & Toxicology June 1, 1999 DOI: 10.1111/j.1600-0773.1999.tb01492.x (opens in new tab)

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Study at a glance

AI-extracted from the abstract
Characteristics Experimental animal study Peer reviewed
Population Dark Agouti rats
Interventions MDEA MDMA
Dose 35 mg/kg intraperitoneally (MDEA), 15 mg/kg intraperitoneally (MDMA)
Duration 7 days
Topics MDMA Serotonin
Keywords Pharmacology Neurotoxicity Hippocampus Hyperthermia Dopamine Striatum Acute toxicity Anesthesia
Citations 26
Key findings MDEA (eve) is less potent than MDMA (ecstasy) in causing acute hyperthermia and serotonin neurotoxicity in rats, but because higher doses of MDEA are probably required for mood effects, the data do not support MDEA as a safer recreational drug.

Abstract

Abstract: 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‐methylenedioxymetham‐phetamine (MDMA or “ecstasy”) of 15 mg/kg intraperitoneally. Seven days later this dose of MDMA produced a marked (50%) loss of 5‐HT and its metabolite 5‐HIAA in cortex, hippocampus and striatum and a similar loss of [ 3 H]‐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 striata! 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.

Comparable studies

Other preclinical and animal studies on MDMA, most cited first.

Study Year Design Participants
Neurotoxicity of the psychedelic amphetamine, methylenedioxymethamphetamine. Rats (implied by typical neurochemical study context) 1987 Experimental study
3,4-Methylenedioxymethamphetamine and 3,4-methylenedioxyamphetamine destroy serotonin terminals in rat brain: quantification of neurodegeneration by measurement of [3H]paroxetine-labeled serotonin uptake sites. Rat brain 1987 Animal experiment
Comparison of the monoamine transporters from human and mouse in their sensitivities to psychostimulant drugs Human and mouse dopamine, norepinephrine, and serotonin transporters expressed in cells 2006 In vitro laboratory study
Small Changes in Ambient Temperature Cause Large Changes in 3,4-Methylenedioxymethamphetamine (MDMA)-Induced Serotonin Neurotoxicity and Core Body Temperature in the Rat Rats 1998 Experimental study
Altered Serotonin Innervation Patterns in the Forebrain of Monkeys Treated with (±)3,4-Methylenedioxymethamphetamine Seven Years Previously: Factors Influencing Abnormal Recovery Squirrel monkeys treated with MDMA 1999 Observational cohort

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