Serotonin function and cerebral glucose metabolism were assessed in rats after either prenatal or post-natal exposure to MDMA. Dams (pregnant female rats) received vehicle or 20 mg/kg MDMA twice daily on four consecutive days, with the first dose of MDMA or vehicle given on gestational day 15. Neonatal rats not exposed to MDMA during gestation received an identical dose regimen (20 mg/kg twice daily for 4 consecutive days), with groups of neonatal rats assigned to receive treatment commencing on postnatal day 10, 15, 20, 25 or 30. Both rats exposed to MDMA during gestation and those receiving MDMA after birth were killed were on post-natal day 40. An identical MDMA regimen was also given to a second group of neonatal rats on post-natal day 90. Serotonin transporter site density was assessed via radioactive paroxetine (a serotonin uptake inhibitor) in prenatally exposed neonatally exposed rats. Cerebral glucose metabolism was measured through autoradiography with radiolabeled 2-deoxyglucose (2-DG) on postnatal day 90, as measured through timed arterial blood samples. Levels of paroxetine binding in rats prenatally exposed to MDMA were similar to levels in control rats. When MDMA treatment was started prior to postnatal day 25, no differences were seen in paroxetine binding in MDMA-treated rats and controls. Paroxetine binding was reduced in rats given a first dose of MDMA on postnatal day 25 or 30, but reduction in paroxetine binding was even greater in rats first given MDMA on postnatal day 90. There was a tendency for elevated cerebral glucose metabolism to occur in rats prenatally exposed to MDMA, but this effect was seen in only 9 of 25 brain areas examined, and included locus coerulus, one section of hippocampus (subiculum), anterior thalamus and hypothalamus. Glucose metabolism was also more variable in rats that had received prenatal exposure to MDMA than in controls. However, in rats exposed MDMA on or after postnatal day 10, there were no differences in metabolism in any brain region examined. Study findings suggest that perinatal exposure to MDMA may affect development of serotonin neurons only when the exposure falls within a specific "critical window." This period of time arises during prenatal exposure and appears again after postnatal day 25. Since body temperature in dams and neonates was not measured, it is unclear whether reductions in serotonin transporter sites are directly related to MDMA exposure or are due at least in part to exposure to hyperthermia. Several research teams have found possible developmental effects of MDMA (Meyer et al. 2002; Whitworth et al. 2002; Won et al. 2002). Humans might face risk of similar developmental effects of MDMA, with the critical window not specified but possibly occurring in late pregnancy, as neonatal rodents are often compared to human fetuses in the third trimester.