Squirrel monkeys given a demonstrably neurotoxic regimen of MDMA failed to show differences in performance on a learning task involving working memory (pressing 1 of four appropriate keys after viewing a specific cue), with task performance measured before and after MDMA or saline administration. MDMA (2.5 mg/kg) or saline was given twice daily for 4 days, with another MDMA regimen (5 mg/kg twice daily in 4 days) given after recording dose-response curves for repeated-acquisition task after each test drug. Monkeys underwent the learning task, presumed to involve attention and working memory, 4 to 14 days after each MDMA regimen, with at least 3 days between administration of each test drug. There were no differences in performance at baseline or after the administration of the serotonergic drugs fenfluramine and m-CPP, or after the benzodiazepine triazolam. All 3 test drugs (fenfluramine, m-CPP and triazolam) decreased response time in MDMA and saline-treated monkeys, and triazolam increased number of errors in both groups of monkeys. All subjects were killed 61 days after MDMA regimen 2, and frontal, parietal, temporal, occipital and hippocampal areas compared for concentration of 5HT, 5HIAA and serotonin transporter. Amount of serotonin in MDMA-treated monkeys ranged from 0.7% (occipital) to 4.7% (frontal) of controls, and SERT ranged from 33.4 (frontal) to 45.2% of control values (parietal). Study findings suggest that the chosen task is insensitive to MDMA-induced neurotoxicity, that serotonin must be further reduced before it affects performance on a repeated acquisition task, or that fenfluramine and m-CPP alter task performance through non-serotonergic means. This study is one of several recently published studies in non-human animals (Fone et al, 2002; Broening 2001) and in humans (Daumann et al. 2001; Fox et al. 2001; Morgan et al. 2002) suggesting at least one, and possibly several, dissocations between indicators of changes in neuropsychological and cognitive function after MDMA / ecstasy and after MDMA-induced neurotoxicity.