{'fraction_non_alphanumeric': 0.02689075630252101, 'fraction_numerical': 0.0058823529411764705, 'mean_word_length': 5.728813559322034, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Reduced in vivo binding to the serotonin transporter in the cerebral cortex of MDMA (‘ecstasy’) users

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 [123I]-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.