Reversibility of ecstasy-induced reduction in serotonin transporter availability in polydrug ecstasy users.
OBJECTIVE
Animal data suggest that the synthetic drug ecstasy may damage brain serotonin neurons. Previously we reported protracted reductions in the availability of the serotonin transporter (SERT), an index of integrity of the axon terminals of brain serotonergic neurons, in SERT-rich brain regions in current human ecstasy users. Comparison of current ecstasy users and former ecstasy users yielded some evidence that this reduction might be reversible. However, participant selection effects could not be ruled out. Therefore, follow-up examinations were performed in these subjects to test the following a priori hypothesis in a prospective longitudinal design that eliminates participant selection effects to a large extent: availability of the SERT increases towards normal levels when ecstasy use is stopped, and remains unchanged or is further decreased if use is continued.


METHODS
Two follow-up positron emission tomography measurements using the SERT ligand [11C](+)McN5652 were completed by 15 current and nine former ecstasy users. All subjects used illicit drugs other than ecstasy, too. The time interval between repeated measurements was about 1 year. The time course of the availability of the SERT was analysed in the following SERT-rich regions: mesencephalon, putamen, caudate and thalamus.


RESULTS
Current ecstasy users showed a consistent increase in the availability of the SERT in the mesencephalon during the study (Friedman test: p = 0.010), which most likely was caused by a decrease in the intensity of ecstasy consumption (Spearman correlation coefficient -0.725, p = 0.002). Former ecstasy users showed a consistent increase in SERT availability in the thalamus (Friedman test: p = 0.006).


CONCLUSIONS
Ecstasy-induced protracted alterations in the availability of the SERT might be reversible.
Buchert
Ralph
R
Department of Nuclear Medicine, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany. buchert@uke.uni-hamburg.de
Thomasius
Rainer
R
Petersen
Kay
K
Wilke
Florian
F
Obrocki
Jost
J
Nebeling
Bruno
B
Wartberg
Lutz
L
Zapletalova
Pavlina
P
Clausen
Malte
M
D000293:Adolescent; D000328:Adult; D001921:Brain / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007546:Isoquinolines / Q000494:pharmacology; D008297:Male; D018817:N-Methyl-3,4-methylenedioxyamphetamine / Q000494:pharmacology*; D009474:Neurons / Q000378:metabolism; D049268:Positron-Emission Tomography / Q000379:methods; D012702:Serotonin Antagonists / Q000494:pharmacology; D050486:Serotonin Plasma Membrane Transport Proteins / Q000096:biosynthesis* / Q000378:metabolism; D019966:Substance-Related Disorders / Q000473:pathology
D007546:Isoquinolines; D012702:Serotonin Antagonists; D050486:Serotonin Plasma Membrane Transport Proteins; C058079:McN 5652; D018817:N-Methyl-3,4-methylenedioxyamphetamine