Journal of Neuroscience
June 15, 1999
George Hatzidimitriou, Una D. Mccann, George A. Ricaurte
338 citations
Seven years after treatment with MDMA (Ecstasy), squirrel monkeys still showed abnormal brain serotonin innervation patterns, though deficits in some regions were less severe than those observed at 18 months. No loss of serotonin nerve cell bodies in the rostral raphe nuclei was found, indicating that the abnormal patterns are not due to the loss of a particular cell group. Factors influencing recovery of injured serotonin axons include the distance of the affected terminal field from the raphe nuclei, the degree of initial injury, and possibly proximity to myelinated fiber tracts. Additional studies are needed to understand these factors and whether findings apply to humans.
Journal of Neuroscience
August 1, 1995
Christina Weide Fischer, George Hatzidimitriou, J Wlos et al.
269 citations
MDMA destroys serotonin axons in the brain. After injury, these axons can regrow, but the new connections are often abnormal. In rats and squirrel monkeys studied 12–18 months after MDMA exposure, some brain regions remained denervated while others became reinnervated or even hyperinnervated. Distant targets like the dorsal neocortex stayed denervated, whereas proximal targets such as the amygdala and hypothalamus recovered. Longer or more highly arborized axons had lower recovery probability. This lasting reorganization of serotonin projections may have implications for humans who use MDMA recreationally.
Science
September 27, 2002
George A. Ricaurte, Jie Yuan, George Hatzidimitriou et al.
179 citations
The recreational drug MDMA (ecstasy) is widely believed to selectively damage serotonin neurons in animals and possibly humans. However, nonhuman primates given several sequential doses of MDMA—a pattern similar to human use—developed severe damage to brain dopamine neurons, along with milder serotonin damage. This dopamine loss was linked to increased vulnerability to movement problems. The findings suggest that recreational MDMA users may unknowingly risk developing neuropsychiatric disorders related to dopamine or serotonin deficiency, either as young adults or later in life.
Synapse
September 5, 2002
Liesbeth Reneman, Jan Booij, Jan B. A. Habraken et al.
33 citations
SPECT imaging with [123I]β-CIT can detect reductions in serotonin transporter density caused by MDMA neurotoxicity. A rhesus monkey treated with MDMA showed a 39% decrease in SERT binding in the hypothalamic/midbrain region 31 days after treatment, matching autoradiography data (−34%). Rat studies confirmed significant binding reductions in SERT-rich regions one week after neurotoxic MDMA doses. The findings validate [123I]β-CIT SPECT as a method for measuring MDMA-induced serotonergic damage in the brain.