Reducedin vivobinding to the serotonin transporter in the cerebral cortex of MDMA (‘ecstasy’) users

Regular use of MDMA ('ecstasy') is associated with reduced binding of the serotonin transporter in the cortex, especially in the primary sensory-motor cortex, while dopamine transporter binding in the lenticular nuclei remains normal. This suggests that MDMA may cause specific, at least temporary, damage to serotonin-producing neurons in humans, which could contribute to psychiatric problems. The study compared ten male regular ecstasy users with ten well-matched controls using SPECT imaging with a serotonin transporter ligand.

Study at a glance

Abstract

Background The use of MDMA (‘ecstasy’) is common among young people in Western countries. Animal models of MDMA toxicity suggest a loss of serotonergic neurons, and potentially implicate it in the development of significant psychiatric morbidity in humans. Aims To test whether long-term use of MDMA can produce abnormalities in cerebral serotonin, but not dopamine, transporter binding measured by single photon emission computed tomography (SPECT) Method Ten male regular ecstasy users and 10 well-matched controls recruited from the same community sources participated in SPECT with the serotonin transporter (SEPT) ligand [ 123 I]-CIT. Dopamine transporter binding was determined from scans acquired 23 hours after injection of the tracer. Results Ecstasy users showed a cortical reduction of SERT binding, particularly prominent in primary sensory-motor cortex, with normal dopamine transporter binding in lenticular nuclei. Conclusions This cross-sectional association study provides suggestive evidence for specific, at least temporary, serotonergic neurotoxicity of MDMA in humans.