α-Lipoic acid prevents 3,4-methylenedioxy-methamphetamine (MDMA)-induced neurotoxicity
Norberto Aguirre, Meritxell Barrionuevo, Marı́a J. Ramı́rez, Joaquı́n Del Rı́o, Berta Lasheras
Neuroreport November 1, 1999 DOI: 10.1097/00001756-199911260-00039 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Rats |
| Interventions | MDMA α-lipoic acid |
| Dose | 20 mg/kg MDMA; 100 mg/kg α-lipoic acid twice daily for 2 days |
| Duration | 1 week after MDMA administration |
| Topics | MDMA Serotonin |
| Keywords | Neurotoxicity Methamphetamine Hippocampus Pharmacology Striatum Hyperthermia Endocrinology |
| Citations | 89 |
| Key findings | Α-lipoic acid prevented MDMA-induced serotonergic deficits and glial changes in rats, supporting free radical involvement in neurotoxicity. |
Abstract
A single administration of 3,4-methylenedioxymetham-phetamine (MDMA, 20 mg/kg, i.p.), induced significant hyperthermia in rats and reduced 5-hydroxytryptamine (5-HT) content and [3H]paroxetine-labeled 5-HT transporter density in the frontal cortex, striatum and hippocampus by 40–60% 1 week later. MDMA treatment also increased glial fibrillary acidic protein (GFAP) immunoreactivity in the hippocampus. Repeated administration of the metabolic antioxidant α-lipoic acid (100 mg/kg, i.p., b.i.d. for 2 consecutive days) 30 min prior to MDMA did not prevent the acute hyperthermia induced by the drug; however, it fully prevented the serotonergic deficits and the changes in the glial response induced by MDMA. These results further support the hypothesis that free radical formation is responsible for MDMA-induced neurotoxicity.