This review of MDMA pharmacology written for neuroscientists, focuses on mechanisms of MDMA neurotoxicity, and includes sections on acute effects of MDMA, neurotoxicity, mechanisms of toxicity, and MDMA effects on fetal development. The authors present a case for MDMA neurotoxicity in non-human animals, and a more cautious case for neurotoxicity in humans, qualified by concerns about limitations in studies of Ecstasy users. The authors discuss findings supporting a role for a number of compounds in producing MDMA neurotoxicity through generating oxidative stress, including MDMA and neurotransmitter metabolites. They briefly discuss the role of hyperthermia in MDMA neurotoxicity. Strong points of the review are its discussion of models of MDMA neurotoxicity. However, elsewhere the paper is incredibly uneven, with indications that the authors are not very familiar with behavioral studies in human and non-human animals. For instance, the authors seem to assume that direct drug actions can be derived from findings in human studies of drug interactions. Findings of gender differences in acute MDMA effects (Liechti and Vollenweider 2001) are considered alongside findings of gender differences in long-term effects on serotonin transporter levels in ecstasy users (Reneman et al. 2001) and referred to within the same paragraph, without noting differences in effects studied. The authors fail to cite a number of controlled studies of MDMA in humans that were almost certainly available to them at the time of writing (Cami et al. 2000; Tancer et al. 2001). While understandable, the authors do not address any acute adverse events beyond hyperthermia, such as psychological distress, liver problems or hyponatremia. In discussing neurocognitive studies, no mention is made of findings of impaired executive function, and the authors fail to note or comment on the apparent domain specificity (verbal) of memory impairments in Ecstasy users. They neither mention nor comment on the studies of psychological problems in ecstasy users (for instance Gamma et al. 2000; Parrott et al. 2002; Morgan et al. 2002). The authors discuss acute neuroendocrine effects after MDMA administration within the section on human MDMA neurotoxicity with no clear linkage between the discussion and this section, aside from the fact that participants were Ecstasy users. When describing mechanisms of MDMA neurotoxicity, the authors fail to clearly explain the role of tryptophan hydroxylase inhibition in neurotoxicity, and they do not mention, support or refute a possible role for energy exhaustion or bionenergetic stress as a MDMA neurotoxicity (see ). This is surprising as there exists considerable research examining this hypothesis, with findings both for and against its role in MDMA neurotoxicity (see, for example, Burrows et al. 2000; Darvesh et al. 2002; Huether et al. 1997). Overall, the review is highly uneven, particularly when the authors move beyond their area of expertise, and partisan in its views on MDMA neurotoxicity, as it only addresses oxidative stress and hyperthermia as agents in MDMA neurotoxicity, and not energy exhaustion.