Controversy exists as to whether MDMA and MDA should be classified with the other hallucinogens. Both MDMA and MDA have structural similarities to the Psychostimulant Amphetamine, and they have amphetamine-like psychostimulant properties. Yet, these designer drugs also have properties in common with LYSERGIC ACID DIETHYLAMIDE (LSD) and MESCALINE; with lower doses, however, they produce fewer perceptual phenomena and less emotional liability, or "keyed-up'' feelings and disturbances of thought, than other hallucinogens, and there tends to be a tranquil state with a feeling that tender emotions are meaningful. As doses are increased, the illusions and other LSD-like phenomena are seen. Because of their mixed effects, MDMA and MDA are sometimes referred to as STIMULANT-hallucinogens.

Unlike LSD, users of MDMA have reported nausea, jaw clenching and teeth grinding, increased

Figure 1

Phenethylamine Hallucinogens

Figure 1

Phenethylamine Hallucinogens muscle tension, and blurred vision, as well as panic attacks. MDMA also causes amphetamine-like stimulation of the autonomic nervous system, producing increases in blood pressure, heart rate, and body temperature. A type of hangover the day after taking MDMA has been described, involving headache, insomnia, fatigue, drowsiness, sore jaw muscles, and loss of balance.

Like the other hallucinogens, the exact mechanisms of action of MDMA are not known. MDMA, like the indole- and phenethylamine-type hallucinogens, binds to receptors for the neurotransmitter serotonin. Thus, many effects might be due to interactions with brain serotonergic systems. MDMA, however, also causes the release of both dopamine and serotonin, so some effects may be related to their stimulant properties.

By the early 1990s, some evidence indicated that MDMA might damage nerve cells. In laboratory experiments, MDMA can produce long-lasting changes in the function of neurons that use serotonin as the neurotransmitter, sometimes causing the death of these cells. Even though LSD also interacts with serotonergic nerve cells, the administration of massive doses of LSD does not damage these cells. In contrast, in experimental animals, a single dose

MDMA (Ecstasy) packaged for bulk distribution. (Drug Enforcement Administration)

of MDMA approximately three times higher than the typical street dose has been shown to affect brain serotonergic systems for several weeks. In some studies, neurochemical markers did not return to normal until one year after drug administration. Moreover, it is not clear whether there was actual regeneration of neurons or only compensatory changes in the remaining undamaged neurons. In these experiments, the neurotoxic effects of MDMA appear to depend on total exposure. Both the dose taken and the number of times the drug is consumed may be related to brain-cell changes. The exact mechanism of MDMA-induced neurotox-icity is unknown at this time and may be due to MDMA itself, or it could involve the formation of a neurotoxic metabolite.

Although there is controversy whether studies utilizing laboratory animals can be extrapolated to human MDMA users, some evidence suggests that brain function can be altered in humans exposed to MDMA. Although the consequences to behavior and thinking caused by damage to the serotonergic nerve cells in young users are unknown, some effects of MDMA-induced toxicity may become apparent as the users age. Cells die as part of the aging process, and if exposure to MDMA kills or weakens a certain proportion of cells, the effects of normal cell loss due to aging might be exacerbated. Serotonergic systems have been implicated in the control of sleep, food intake, sexual behavior, anxiety, and mood. Thus, serotonergic cell loss could have major consequences.

(SEE ALSO: Complications: Mental Disorders; Dopamine; Methamphetamine; Serotonin)


Barnes, D. M. (1988). New data intensify the agony over ecstasy. Science, 239, 864-866. Glennon, R. A. (1987). Psychoactive phe-nylisopropylamines. In H. Y. Meltzer (Ed.), Psycho-pharmacology: The third generation of progress. New York: Raven Press. Ricaurte, G., ET AL. (1985). Hallucinogenic amphetamine selectively destroys brain serotonin nerve terminals. Science, 229, 986-998. SHULGIN, A., & SHULGIN, A. (1991). PIHKAL: A chemical love story. Berkeley, CA: Transform Press.

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