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Effect of ascorbate and cysteine on the 3,4-methylenedioxymethamphetamine-induced depletion of brain serotonin.

G A Gudelsky

Journal of neural transmission (Vienna, Austria : 1996) 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.