Neurotoxic damage of central serotonergic systems has been demonstrated in numerous animal studies after exposure to methylenedioxyamphetamines (ecstasy). (Battaglia et al. 1987Molliver et al. 1990;O'Hearn et al. 1988;Ricaurte et al. 1985Ricaurte et al. , 1988Ricaurte et al. , 1992Schmidt et al. 1987, Wilson et al. 1989. Notably, monkeys seem to be more susceptible to the neurotoxic effects of ecstasy than lower mammals. Although recovery from neurotoxic damage was almost complete in most rats after 12 months, in nonhuman primates, neurotoxic brain alterations were still detectable as long as 18 months after MDMA-exposure Fischer et al. 1995;Ricaurte et al. 1988Ricaurte et al. , 1992. The lowest MDMA dose, which elicited long-term structural damage in serotonergic neurons of nonhuman primates, was 5mg/kg SC twice daily for 4 days . Although some heavy users take ecstasy in quantities that approach those experimental doses, the ma- Received May 25, 1999; revised October 20, 1999; accepted October 27, 1999. N EUROPSYCHOPHARMACOLOGY 2000 -VOL . 22 , NO . 6 Auditory Evoked Source Activity in Ecstasy Users 609 jority of recreational users do not. However, the threshold dose for human neurotoxicity is not clear, and humans may be more susceptible than primates. In addition, it is possible that the cumulative doses ingested by typical recreational users over a longer period of regular use bear a similar neurotoxic risk as high experimental doses administered within a short period of time.In a recent positron emission tomography (PET) study with the selective 5-HT transporter ligand McN-5652, abstinent ecstasy users showed decreased brain 5-HT transporter binding as compared with controls, and this decrease correlated with the extent of previous ecstasy use . Hence, this finding probably reflects neurotoxic brain damage. Serotonergic systems are involved in numerous functions including regulation of mood and drive, cognition, vegetative function, pain, and neuroendocrine secretion. So far, mild memory impairments (Bolla et al. 1998;Krystal et al. 1992;Morgan 1999), elevated impulsivity (Morgan 1998) and neuroendocrine abnormalities (Gerra et al. 1998;Price et al. 1989) have been demonstrated in abstinent ecstasy users. In addition, depressive and anxiety disorders after ecstasy use might also reflect, at least in part, a neurotoxic serotonergic damage (Benazzi and Mazzoli 1991;Gouzoulis-Mayfrank et al. 1996;Green et al. 1995;McCann and Ricaurte 1991;McGuire et al. 1994;Pallanti and Mazzi 1992).The aim of our investigation was to study an aspect of information processing in abstinent ecstasy users, which is thought to reflect the level of central serotonergic neurotransmission (Hegerl and Juckel 1993). For this purpose, we recorded auditory evoked potentials (AEP) and used the method of dipole source analysis. An old debate exists on the dependence of the amplitude of sensory evoked potentials on stimulus intensity (Buchsbaum and Silverman 1968; review in: Carillo-dela-Pena 1992;Von Knorring and Perris 1981;Von Kn...

The popular recreational drug Ecstasy (3,4-methylenedioxymethamphetamine, or MDMA, and related congeners) is neurotoxic upon central serotonergic systems in animal studies. So far, the most convincing evidence for neurotoxicity-related functional deficits in humans derives from neurocognitive studies demonstrating dose-related memory problems in Ecstasy users. The aim of the current investigation was to study the relationship between the psychological profile of recreational Ecstasy users and the patterns of their drug use. Twenty-eight abstinent recreational Ecstasy users with concomitant use of cannabis only and two equally sized, matched groups of cannabis users and non-users were administered standardized self-rating scales for the assessment of psychological problems which are thought to be related to central serotonergic function. Ecstasy users had elevated scores on subscales measuring impulsiveness, anxiety, sensation seeking, somatic complaints, obsessive-compulsive behavior and psychoticism. Higher scores were associated with both heavier Ecstasy and heavier cannabis use. After controlling for cannabis use, most group differences in psychometric scores no longer achieved statistical significance. The present data are in line with other reports demonstrating a broad range of psychological problems in Ecstasy users. However, the concomitant use of other drugs, specifically cannabis, seems to be crucial in this respect. Therefore, compared with cognitive deficits, psychological problems appear to be less suitable functional indices of Ecstasy-related neurotoxic damage of central serotonergic systems in humans. Copyright 2001 John Wiley & Sons, Ltd.

No abstract

No abstract

No abstract