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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, A. Richard Green

Pharmacology & Toxicology June 1, 1999 DOI: 10.1111/j.1600-0773.1999.tb01492.x via OpenAlex

Summary

AI-generated from the abstract

A single dose of the recreational drug MDEA ("eve") given to Dark Agouti rats caused an acute, dose-dependent rise in body temperature. The peak hyperthermia from 35 mg/kg of MDEA matched that from 15 mg/kg of MDMA ("ecstasy"). Seven days later, MDMA caused a 50% loss of serotonin and its metabolite in the cortex, hippocampus, and striatum, indicating neurotoxic damage to serotonin nerve endings. MDEA at the highest dose produced only a 20% loss in cortex and hippocampus and no loss in striatum, with weak dose dependence. Neither drug altered striatal dopamine. MDEA had about half the potency of MDMA for hyperthermia and one-quarter the potency for serotonin neuron degeneration.

Study at a glance

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 Chemistry Neurotoxicity
Citations 26
Key finding 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.

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