Introduce this activity using Powerpoint slides and teaching scripts from the National Institute on Drug Abuse web site (http://www.drugabuse.gov/pubs/Teaching/). Use all or part of the slide show entitled “The Brain and the Actions of Cocaine, Opiates, and Marijuana” to review the brain, neurons, neural communication, and drug effects. Use another slide show entitled “The Neurobiology of Ecstasy (MDMA)” to describe MDMA use specifically. For more information, consult Brain Facts or Neuroscience (see References).

“Ecstasy” is 3,4-methylenedioxymethamphetamine, and is also known as MDMA, XTC, X, Adam, Clarity, or Lover’s Speed. MDMA is a synthetic chemical similar in structure to methamphetamine. Usually taken in pill or capsule form, its psychological effects last approximately 3-6 hours and include euphoria, alertness, heightened sense of touch, and empathy for other individuals (Burgess et al. 2000, Gudelsky & Yamamoto 2003). Immediate negative responses can also occur, such as headaches, jaw clenching, blurred vision, nausea, and mental problems (impaired judgment, confusion, anxiety, or sleep disruption). MDMA can also increase heart rate and blood pressure. Dilated pupils sometimes indicate drug use. Several days after these initial effects, users report feeling sad, unsociable, and irritated.

Even a single dose of MDMA can have life-threatening effects. In 2001, approximately 5500 emergency room visits involved MDMA-related cases of dangerously high body temperature, dehydration, hypertension, heart attack, stroke, muscle breakdown, kidney failure, seizures, and cerebral hemorrhage. (See SAMHSA website for more statistics.) Overheated and overcrowded conditions (as found in “raves”) exacerbate these problems.

Long-lasting, perhaps permanent, damage to nerve terminals and axons occurs after MDMA use. The drug causes degradation of nerve terminals and axons that secrete the neurotransmitter called serotonin (Gudelsky & Yamamoto 2003, Burgess et al. 2000). Evidence of such damage is observable in the brains of human MDMA users, via the brain imaging technique known as Positron Emission Tomography . Low levels of serotonin are involved in many disorders, including depression, anxiety, impulsivity, and sleep abnormalities.
Both short- and long-term effects of MDMA relate to its ability to increase the amount of neurotransmitter in the synapse. Due to similarities in chemical structure, MDMA replaces several neurotransmitters (serotonin, dopamine, and norepinephrine) at reuptake sites where the neurotransmitters would normally be recycled back into the axon terminal. This causes the neurotransmitters themselves to remain in the synapse longer than usual and continue binding with postsynaptic receptor proteins. What’s more, MDMA itself can be transported into the axon terminal where it causes even more neurotransmitter release.

Finally, MDMA causes degeneration of serotonin axons. By releasing so much serotonin, MDMA weakens the axon terminal. MDMA also causes “superoxidation” (in a way “rusting” the serotonin axon), and excess calcium release inside neurons. Together these processes cause serotonin axons to die off. Without axons, serotonin neurons cannot communicate with other neurons, and thereby may contribute to the long-term detrimental effects of MDMA on behavior, cognition, and mood. Overall, it is clear that MDMA is not safe and can damage the nervous system.