Effect of ascorbate and cysteine on the 3,4-methylenedioxymethamphetamine-induced depletion of brain serotonin.
Journal of Neural Transmission 1996 DOI: 10.1007/bf01271253 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Controlled experimental animal study Peer reviewed |
|---|---|
| Population | Rats |
| Interventions | MDMA sodium ascorbate L-cysteine |
| Dose | MDMA 20 mg/kg s.c.; sodium ascorbate 250 mg/kg i.p.; L-cysteine 500 mg/kg i.p. |
| Duration | Serotonin measured 7 days after MDMA; antioxidants given 30 min before and 5 hrs after MDMA |
| Measures | striatal serotonin concentration, in vivo microdialysis |
| Topics | MDMA Serotonin |
| Key findings | A single MDMA injection (20 mg/kg) reduced striatal serotonin by 30-35% at seven days in rats, but this reduction was not significant when rats received the antioxidants sodium ascorbate or L-cysteine before and after MDMA. The antioxidants did not affect brain MDMA accumulation or MDMA-stimulated dopamine release. The authors argue these results support the view that MDMA-induced serotonin neuron toxicity may involve free radicals and oxidative damage. |
Abstract
The extent of long-term depletion of serotonin (5-HT) produced by 3,4-methylenedioxymethamphetmaine (MDMA) was assessed in rats treated with the antioxidants sodium ascorbate or L-cysteine. There was a 30-35% reduction in the striatal concentration of 5-HT 7 days following a single injection of MDMA (20 mg/kg, s.c.). MDMA had no significant effect on striatal concentrations of 5-HT in rats that had been treated with ascorbate (250 mg/kg, i.p.) or cysteine (500 mg/kg, i.p.) 30 min prior to and 5 hrs following the administration of MDMA. Treatment with ascorbate or cysteine did not alter the accumulation of MDMA in brain as determined by in vivo microdialysis. Moreover, neither ascorbate nor cysteine altered the stimulation of dopamine release elicited by MDMA. These data are supportive of the view that MDMA-induced toxicity of 5-HT neurons may be related to the production of free radicals and subsequent oxidative damage.
Comparable studies
Other preclinical and animal studies on MDMA, most cited first.
Citations in the library
Cited by 22
- Small Changes in Ambient Temperature Cause Large Changes in 3,4-Methylenedioxymethamphetamine (MDMA)-Induced Serotonin Neurotoxicity and Core Body Temperature in the Rat Journal of Neuroscience July 1, 1998
- Neurotoxicity of Methamphetamine and 3,4-methylenedioxymethamphetamine Life Science July 24, 2013
- Ascorbic acid prevents 3,4-methylenedioxymethamphetamine (MDMA)-induced hydroxyl radical formation and the behavioral and neurochemical consequences of the depletion of brain 5-HT Synapse 2001
- Analysis of Ecstasy (MDMA)‐induced transcriptional responses in the rat cortex The FASEB Journal December 1, 2002
- Studies on the mechanisms underlying amiloride enhancement of 3,4-methylenedioxymethamphetamine-induced serotonin depletion in rats. European Journal of Pharmacology May 21, 2007
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Cites 13
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- Neurotoxicity of the psychedelic amphetamine, methylenedioxymethamphetamine. Journal of Pharmacology and Experimental Therapeutics 1987
- Potentiation of 3,4-methylenedioxymethamphetamine-induced dopamine release and serotonin neurotoxicity by 5-HT2 receptor agonists. European Journal of Pharmacology November 3, 1994
- Blockade of Striatal 5‐Hydroxytryptmine2Receptors Reduces the Increase in Extracellullar Concentrations of Dopamine Produced by the Amphhetamine analogue 3,4‐Methylenedioxymethamphetamine Journal of Neurochemistry April 1, 1994
- The monoamine oxidase-B inhibitor L-deprenyl protects against 3,4-methylenedioxymethamphetamine-induced lipid peroxidation and long-term serotonergic deficits. Journal of Pharmacology and Experimental Therapeutics May 1, 1995
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