Serotonergic deficits and impaired passive-avoidance learning in rats by MDEA: a comparison with MDMA.
Meritxell Barrionuevo, Norberto Aguirre, J D Del Río, Berta Lasheras
Pharmacology, biochemistry, and behavior February 2000 DOI: 10.1016/s0091-3057(99)00170-7 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Experimental animal study Peer reviewed |
|---|---|
| Population | Rats |
| Interventions | MDEA MDMA WAY 100635 8-OH-DPAT |
| Dose | MDEA 10, 20, or 40 mg/kg IP; repeated 40 mg/kg IP b.i.d. for 4 days; MDEA 20 mg/kg IP before training; MDMA dose not specified |
| Duration | 7 days after single or repeated administration |
| Measures | 5-HT content, 5-HT transporter density, 5-HT1A receptor density, plasma corticosterone levels, passive-avoidance retention performance |
| Topics | MDMA Serotonin |
| Key findings | Repeated MDEA administration (40 mg/kg b.i.d. for 4 days) caused marked long-term reductions in 5-HT content and transporter density, while single doses only at 40 mg/kg had similar effects. MDEA-induced retention deficits were not blocked by WAY 100635, indicating they were not mediated by 5-HT1A receptor activation. |
Abstract
The serotonergic deficits induced by 3,4-methylenedioxyethamphetamine (MDEA, "eve"), were examined and compared with 3,4 methylenedioxymethamphetamine (MDMA, "ecstasy"). A single dose of MDEA (10, 20, or 40 mg/kg IP) induced a dose-related hyperthermia, but only the highest dose significantly reduced 5-HT content and 5-HT transporter density in the frontal cortex and in the hippocampus 7 days later. Long-term serotonergic deficits were much more marked when MDEA was given repeatedly (40 mg/kg IP., b.i.d., for 4 consecutive days). Single or repeated administration of MDEA induced no change on 5-HT1A receptor density in the frontal cortex, brain stem, or hippocampus, although 3 h after both treatments plasma corticosterone levels were significantly increased. MDEA (5-20 mg/kg, IP) produced significant retention deficits in a passive-avoidance learning task. Conversely, 7 days after the repeated administration of MDEA (40 mg/kg b.i.d., for 4 consecutive days) no effect on passive-avoidance performance was observed unless rats were treated again with another dose of MDEA (20 mg/kg IP) 30 min before the training trial. The 5-HT1A receptor antagonist, WAY 100635, prevented the impairment in retention performance induced by 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), but not by MDEA or MDMA, indicating that the effect of these amphetamine derivates was not mediated by 5-HT1A receptor activation. The results suggest the risk of serotonergic dysfunction associated with MDEA abuse in humans.