Memantine prevents the cognitive impairment induced by 3,4-methylenedioxymethamphetamine in rats.
Jorge Camarasa, José M Marimón, Teresa Rodrigo, Elena Escubedo, David Pubill
European Journal of Pharmacology July 28, 2008 DOI: 10.1016/j.ejphar.2008.05.014 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Animal experimental study Peer reviewed |
|---|---|
| Population | Male Long Evans rats (behavioral testing) and mice (locomotor testing) |
| Interventions | Memantine 3 |
| Measures | Object recognition test, Morris water maze |
| Topics | MDMA |
| Key findings | MDMA impaired object recognition and spatial memory in rats, and pre-treatment with memantine prevented both impairments; memantine alone also improved learning. In mice, memantine inhibited MDMA-induced rearing and thigmotaxis. The authors conclude memantine may offer a first approach to treating long-term cognitive deficits in ecstasy users. |
Abstract
Amphetamine abuse is an important risk factor for the development of cognitive impairment involving learning and memory. Since in previous studies we have demonstrated the effectiveness of alpha-7 nicotinic receptor antagonists in preventing the neurotoxicity induced by amphetamine derivatives, the present paper seeks to determine whether pre-treatment with memantine (MEM) (an antagonist of both nicotinic and NMDA receptors) counteracts the memory impairment induced by 3,4-methylenedioxymethamphetamine (MDMA or ecstasy) administration in male Long Evans rats. In mice, MDMA and MEM induced a locomotor stimulant response but with a different profile. Moreover, MEM inhibited the rearing and thygmotaxis behaviour induced by MDMA. Non-spatial memory was tested in the object recognition test and the spatial learning and memory was tested in the Morris water maze. In our experimental conditions, rats receiving MEM pre-treatment recovered the ability to discriminate between the familiar and the novel object that had been abolished by MDMA treatment. Animals treated with MDMA showed impaired learning in the Morris water maze. Results of the probe trial demonstrated that MDMA-treated rats did not remember the location of the platform, but this memory impairment was also prevented by the MEM pre-treatment. Moreover, MEM alone improved the learning task. No differences were observed between the different groups as regards swim speed. In conclusion, MEM significantly improved the learning and memory impairment induced by MDMA and constitutes the first approach to the treatment of the long-term cognitive deficits found in ecstasy users.
Comparable studies
Other preclinical and animal studies on MDMA, most cited first.
Citations in the library
Cited by 14
- The intriguing effects of ecstasy (MDMA) on cognitive function in mice subjected to a minimal traumatic brain injury (mTBI). Psychopharmacology April 1, 2011
- Memory impairment and hippocampus specific protein oxidation induced by ethanol intake and 3, 4‐Methylenedioxymethamphetamine (MDMA) in mice Journal of Neurochemistry March 25, 2013
- Involvement of NMDA glutamate receptors in the acquisition and reinstatement of the conditioned place preference induced by MDMA Behavioural Pharmacology May 14, 2015
- Acute MDMA and Nicotine Co-administration: Behavioral Effects and Oxidative Stress Processes in Mice Frontiers in Behavioral Neuroscience August 2, 2018
- Neuronal Nicotinic Receptors as New Targets for Amphetamine-Induced Oxidative Damage and Neurotoxicity Pharmaceuticals June 15, 2011
and 9 more in the library
Cites 16
- Memory impairment in abstinent MDMA ("Ecstasy") users Neurology December 1, 1998
- Impaired cognitive performance in drug free users of recreational ecstasy (MDMA) Journal of Neurology, Neurosurgery, and Psychiatry June 1, 2000
- (±)3,4-Methylenedioxymethamphetamine (‘Ecstasy’)-Induced Serotonin Neurotoxicity: Studies in Animals Neuropsychobiology 2000
- Memory impairment in abstinent MDMA (“Ecstasy”) users: A longitudinal investigation Neurology April 10, 2001
- A review of chemical agents in the pharmacotherapy of addiction. Current Medicinal Chemistry October 1, 2002
and 11 more in the library