Attenuation of ecstasy-induced neurotoxicity by N-acetylcysteine.
Sara Soleimani Asl, Bita Saifi, Abolhasan Sakhaie, Somayeh Zargooshnia, Mehdi Mehdizadeh
Metabolic Brain Disease February 2015 DOI: 10.1007/s11011-014-9598-0 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Controlled animal experiment Peer reviewed |
|---|---|
| Sample size | 28 |
| Population | Adult male Sprague-Dawley rats (200-250 g) |
| Interventions | MDMA N-acetylcysteine (NAC) |
| Dose | 10 mg/kg MDMA; 100 mg/kg NAC |
| Measures | Morris Water Maze (MWM), Bcl-2 and Bax expression |
| Topics | MDMA |
| Key findings | NAC treatment attenuated MDMA-induced spatial memory deficits in rats, reducing distance traveled and escape latency in the Morris Water Maze and restoring time spent in the target quadrant. NAC also protected against MDMA-induced apoptosis and normalized Bax and Bcl-2 expression in the hippocampus. The authors suggest NAC might be useful for treating neurotoxicity in MDMA users. |
Abstract
Exposure to 3, 4-methylenedioxymethamphetamine (MDMA) can lead to spatial memory impairments and hippocampal cell death. Numerous evidence indicates that the antioxidant N-acetylcysteine (NAC) exerts protective effects in the brain. The present study evaluates the effects of NAC on MDMA-induced neurotoxicity. We intraperitoneally injected 28 adult male Sprague-Dawley rats (200-250 g) with either 0, 10 mg/kg of MDMA, or 10 mg/kg of MDMA plus 100 mg/kg of NAC. Spatial memory was assessed with a Morris Water Maze (MWM). At the end of the study, rats' brains were removed to study the structure and ultrastructure of CA1, and measure Bcl-2 and Bax expressions in the hippocampus. In the MWM, NAC treatment significantly attenuated the MDMA-induced increase in distance traveled (p < 0.05) and escape latency (p < 0.001). The decreased time spent in the target quadrant in MDMA-treated animals was attenuated by NAC (p < 0.01). NAC significantly protected against MDMA-induced apoptosis and the up- and down-regulation of Bax and Bcl-2, respectively. These data have suggested that NAC could protect against behavioral changes and apoptosis in the hippocampus following administration of MDMA. NAC might be useful for the treatment of neurotoxicity in MDMA users.
Comparable studies
Other preclinical and animal studies on MDMA, most cited first.
Citations in the library
Cited by 8
- 3,4-methylenedioxymethamphetamine (MDMA) impairs the extinction and reconsolidation of fear memory in rats. Physiology & Behavior February 1, 2019
- MDMA treatment paired with a trauma-cue promotes adaptive stress responses in a translational model of PTSD in rats Translational Psychiatry May 3, 2022
- Lysosomal Dysfunction and Autophagy Blockade Contribute to MDMA-Induced Neurotoxicity in SH-SY5Y Neuroblastoma Cells. Chemical Research in Toxicology April 20, 2020
- MDMA-Associated Liver Toxicity: Pathophysiology, Management, and Current State of Knowledge. AACN advanced critical care 2019
- Treadmill exercise alters ecstasy- induced long- term potentiation disruption in the hippocampus of male rats. Metabolic Brain Disease October 2017
and 3 more in the library
Cites 16
- Cognitive performance in recreational users of MDMA or 'ecstasy': evidence for memory deficits Journal of Psychopharmacology 1998
- Recreational use of 3,4-methylenedioxymethamphetamine (MDMA) or ‘ecstasy’: evidence for cognitive impairment Psychological Medicine May 1, 2001
- The abused drug MDMA (Ecstasy) induces programmed death of human serotonergic cells The FASEB Journal February 1, 1997
- The Nature of 3, 4-Methylenedioxymethamphetamine (MDMA)-Induced Serotonergic Dysfunction: Evidence for and Against the Neurodegeneration Hypothesis Current Neuropharmacology March 1, 2011
- Damage of serotonergic axons and immunolocalization of Hsp27, Hsp72, and Hsp90 molecular chaperones after a single dose of MDMA administration in Dark Agouti rat: Temporal, spatial, and cellular patterns The Journal of Comparative Neurology 2006
and 11 more in the library