The Effects of Ecstasy or MDMA on the Brain

20140 Ecstasy

The Effects of Ecstasy or MDMA on the Brain

The chemical name for ecstasy is 3,4-methylenedioxymethamphetamine, or MDMA. The chemical structure and the effects of MDMA are similar to amphetamine (a stimulant) and to mescaline (a hallucinogen).

What’s sold as ecstasy often contains drugs other than MDMA, which may or may not be similar in effect to MDMA. Some of the other drugs include caffeine, ephedrine, amphetamine, dextromethorphan, ketamine, and LSD. Ecstasy sometimes contains highly toxic drugs, such as paramethoxyamphetamine (PMA), which can be lethal even in low doses.

MDMA was patented in 1913 and has been used experimentally, most notably as a supplement to psychotherapy in the 1970s. It was made illegal to possess, traffic, import or produce MDMA in Canada in 1976 and in the United States in 1985.

Where does it come from?

Ecstasy is made in illegal labs with chemicals and processes that vary from lab to lab. What’s sold as ecstasy often contains unknown drugs or other fillers.

What does it look ?

Ecstasy is usually sold as a tablet or capsule that is swallowed. It may also be sold in powder form, or the tablets may be crushed and then snorted. There are also rare reports of the drug being injected.

Ecstasy tablets come in different shapes, sizes and colours, and are often stamped with a logo, such as a butterfly or clover, giving them a candy- look. This “branding” of ecstasy tablets should not be mistaken for an indication of quality, as manufacturers may use the same logo, and low-quality copycats are common. Tablets that are sold as ecstasy may not contain MDMA.

Who uses it?

The increased use of ecstasy as a recreational drug began in the 1980s in the United States. Young people at raves (all-night dance parties) were the group most commonly associated with ecstasy use. While still used by young people in clubs and at parties, ecstasy is now also used by a wider range of people in a variety of settings.

A survey of Ontario students in grades 7 to 12 reported a decline in past-year use of ecstasy from six per cent in 2001 to 3.2 per cent in 2009. A 2008 survey of Canadians (aged 15+) reported that 1.4 per cent had used ecstasy at least once in the past year.

How does it make you feel?

How ecstasy affects you depends on several things:

  • your age and your body weight
  • how much you take and how often you take it
  • how long you’ve been taking it
  • the method you use to take the drug
  • the environment you’re in
  • whether or not you have certain pre-existing medical or psychiatric conditions
  • whether you’ve taken any alcohol or other drugs (illegal, prescription, over-the-counter or herbal).

In low to moderate doses, ecstasy can produce feelings of pleasure and well-being, increased sociability and closeness with others. all stimulant drugs, ecstasy can make users feel full of energy and confidence.

Even at low doses, ecstasy can also have strong negative effects. Higher doses are unly to enhance the desirable effects, and may intensify the negative effects. These effects include grinding of teeth and jaw pain, sweating, increased blood pressure and heart rate, anxiety or panic attacks, blurred vision, nausea, vomiting and convulsions.

After the initial effects of the drug have worn off, users may also experience after-effects such as confusion, irritability, anxiety, paranoia, depression, memory impairment or sleep problems.

How long does the feeling last?

The effects of ecstasy usually begin within an hour, and may last four to six hours. The duration of the after-effects cannot be predicted as precisely, though they may last for days or weeks.

Is it addictive?

It’s not uncommon for ecstasy to take on an exaggerated importance in people’s lives. Signs of addiction include strong cravings for the effects of the drug, taking more of the drug than intended, and continuing to use the drug despite the problems it may cause.

Tolerance to ecstasy builds up very quickly. This means the more often you take ecstasy, the less effect the drug has. Taking more of the drug may not achieve the desired results, as frequent ecstasy use depletes serotonin and other brain chemicals that give the ecstasy “high.”

There is little evidence to indicate that MDMA can produce physical dependence or withdrawal symptoms.

Is it dangerous?

It can be. Although some people regard ecstasy as a relatively safe drug, a growing number of deaths have been associated with it. As with many illegal drugs, these risks increase with the amount taken and frequency of use.

A major factor in many ecstasy-related deaths is the dehydration and overheating that can result when ecstasy is taken in conjunction with all-night dancing. Ecstasy increases body temperature, blood pressure and heart rate, which can lead to kidney or heart failure, strokes and seizures. Ecstasy may cause jaundice and liver damage.

People with high blood pressure, heart or liver problems, diabetes, epilepsy or any mental disorder are the most vulnerable to the potential dangers of ecstasy. Part of the danger is that people may not be aware that they have these conditions, and the effects of ecstasy can trigger symptoms.

As with all illegal street drugs, the purity and strength of ecstasy can never be accurately gauged. When you take ecstasy, you don’t know what you’re taking, or how it will affect you.

Combining ecstasy with other drugs, whether illegal or prescription, may cause a toxic interaction. Several prescription medications are known to interact with ecstasy, including a type of antidepressant called monoamine oxidase inhibitors (MAOIs) and ritonavir, a protease inhibitor used to treat HIV.

Driving or operating machinery while under the influence of ecstasy, or any drug, increases the risk of physical injury to the user and others.

What are the long-term effects of using it?

Animal research has established that ecstasy use can damage the brain cells that release serotonin. Research on humans is limited, but there is some evidence to suggest that ecstasy can damage the cells and chemistry of the human brain, affecting functions such as learning and memory.

The risk of damage caused by ecstasy use may be linked to the amount taken and the frequency of use. However, some research suggests that even occasional use of small amounts of ecstasy may damage the brain cells that release serotonin, and that these effects may be long lasting. It is not known whether these effects may be permanent.

Copyright © 2001, 2010 Centre for Addiction and Mental Health

Where can I find more information?


Repeated exposure to MDMA triggers long-term plasticity of noradrenergic and serotonergic neurons

The Effects of Ecstasy or MDMA on the Brain

Repeated exposure to MDMA triggers long-term plasticity of noradrenergic and serotonergic neurons

  • Addiction
  • Synaptic transmission

3,4-Methylenedioxymethamphetamine (MDMA or ‘ecstasy’) is a psychostimulant drug, widely used recreationally among young people in Europe and North America.

Although its neurotoxicity has been extensively described, little is known about its ability to strengthen neural circuits when administered in a manner that reproduces human abuse (i.e. repeated exposure to a low dose). C57BL/6J mice were repeatedly injected with MDMA (10 mg kg−1, intraperitoneally) and studied after a 4-day or a 1-month withdrawal.

We show, using in vivo microdialysis and locomotor activity monitoring, that repeated injections of MDMA induce a long-term sensitization of noradrenergic and serotonergic neurons, which correlates with behavioral sensitization.

The development of this phenomenon, which lasts for at least 1 month after withdrawal, requires repeated stimulation of α1B-adrenergic and 5-hydroxytryptamine (5-HT)2A receptors.

Moreover, behavioral and neuroendocrine assays indicate that hyper-reactivity of noradrenergic and serotonergic networks is associated with a persistent desensitization of somatodendritic α2A-adrenergic and 5-HT1A autoreceptor function.

Finally, molecular analysis including radiolabeling, western blot and quantitative reverse transcription-polymerase chain reaction reveals that mice repeatedly treated with MDMA exhibit normal α2A-adrenergic and 5-HT1A receptor binding, but a long-lasting downregulation of Gαi proteins expression in both locus coeruleus and dorsal raphe nucleus. Altogether, our results show that repeated MDMA exposure causes strong neural and behavioral adaptations and that inhibitory feedback mediated by α2A-adrenergic and 5-HT1A autoreceptors has an important role in the physiopathology of addictive behaviors.

3,4-Methylenedioxymethamphetamine (MDMA), commonly known as ‘ecstasy’, is a substituted amphetamine with psychostimulant and hallucinogenic properties.

This illicit drug is extensively consumed by teenagers and young people in clubs and rave parties, despite the increasing evidence of its putative neurotoxicity1, 2, 3 and its adverse effects on mental health.

Indeed, chronic use of MDMA has been associated with many psychiatric disorders including anxiety, depression or psychosis,4, 5, 6 and may lead to addiction in vulnerable individuals.7

In rodents, MDMA induces locomotor hyperactivity and repeated injections result in behavioral sensitization.8, 9, 10 This long-lasting phenomenon is thought to have a critical role in the development of compulsive drug seeking and drug taking, as well as in cue-induced relapse.11, 12

Studies of the brain circuits underlying addictive behaviors have focused on the mesolimbic dopaminergic system,13, 14 as it was shown that all drugs of abuse, including MDMA, increase extracellular dopamine levels in the nucleus accumbens of rodents.15, 16, 17, 18 However, several in vitro studies indicate that MDMA shows higher affinity for both norepinephrine and serotonin transporters than for dopamine transporter.19, 20, 21

Moreover, growing evidence suggests that the involvement of both noradrenergic and serotonergic systems in MDMA-induced addictive behaviors may have been seriously underestimated.

The pharmacological blockade of either α1-adrenergic or 5-hydroxytryptamine (5-HT)2A receptors reduces the hyperlocomotor effects of MDMA and prevents the development of behavioral sensitization.

22, 23 Also, self-administration of MDMA is abolished in mice lacking the serotonin transporter (serotonin transporter KO mice),24 whereas mice lacking 5-HT2A receptors (5-HT2A KO mice) are insensitive to MDMA-induced reinforcement and cue-induced reinstatement of MDMA-seeking behaviors.25

Recently, we identified a new kind of neural plasticity that may be involved in the long-term behavioral effects of drugs of abuse.

Indeed, we showed that repeated administration of amphetamine, cocaine, morphine, ethanol or nicotine+monoamine oxidase inhibitor induces long-lasting sensitization of noradrenergic and serotonergic neurons in C57BL/6J mice.

26, 27, 28, 29 Molecular mechanisms underlying this phenomenon remain however unknown.

The main purpose of this study was to investigate the long-term effects of a repeated MDMA exposure on noradrenergic and serotonergic transmissions.

The reactivity of noradrenergic and serotonergic neurons was investigated by in vivo microdialysis in the prefrontal cortex (PFC) and behavioral effects were recorded in parallel.

The mechanisms underlying MDMA-induced changes were then investigated at the molecular, physiological and behavioral levels.

Animals were 2–3 months old (26–32 g) C57BL/6J male mice (Charles River, L'Arbresle, France). They were housed eight per cage and maintained on a 12 h light/dark cycle with food and water available ad libitum.

Seven hundred mice were used in this study (300 mice for the microdialysis experiments, 256 mice for the behavioral experiments, 80 mice for the neuroendocrine experiments and 64 mice for the molecular experiments). Each mouse was naive at the beginning of each experiment and was not used repeatedly for the different tests.

Animal experimentation was conducted in accordance with the guidelines for care and use of experimental animals of the European Economic Community (86/809).


3,4-Methylenedioxymethamphetamine (MDMA) hydrochloride, D-amphetamine sulfate, p-chloroamphetamine (PCA) hydrochloride, prazosin hydrochloride, WAY-100635 (N-[2-[4-(2-[O-methyl-3H]methoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridinyl) cyclohexane carboxamide trihydrochloride) hydrochloride and efaroxan hydrochloride were purchased from Sigma-Aldrich (L’Isle d’Abeau-Chesne, France). Dexmedetomidine hydrochloride was purchased from Tocris Bioscience (Bristol, UK). SR46349B hemifumarate was a generous gift from Sanofi-Aventis (Paris, France) and F13640 was kindly supplied by Pierre Fabre Laboratories (Castres, France). All drugs were dissolved in saline (0.9% NaCl) except prazosin, which was dissolved and sonicated in water (50% of final volume), and then completed with saline and SR46349B, which was dissolved and sonicated in saline plus lactic acid (0.1%), and then finally neutralized with 10 M NaOH. Doses are expressed as salts. MDMA was given at 10 mg kg−1.10 D-amphetamine was given at 2 mg kg−1 and PCA at 7 mg kg−1.26 Doses of prazosin (1 mg kg−1) and SR46349B (1 mg kg−1) were identical to those used in previously reported experiments.26 Efaroxan was given at 2.5 mg kg−1 and WAY-100635 was given at 1 mg kg−1. The dose of F13640 given was between 0.1 and 0.6 mg kg−1 (ref. 30) and of dexmedetomidine was between 0.1 and 0.5 mg kg−1.31 In systemic experiments, drugs were injected intraperitoneally (0.1 ml per mouse). In local experiments, drugs were dissolved in artificial cerebrospinal fluid (see below) at a concentration of 1–1000 μM and infused incrementally in the PFC, the LC or the dorsal raphe nucleus (DRN) through the dialysis probe.

Repeated treatment

Mice were given four consecutive daily injections of saline or MDMA in the cylindrical compartment used for microdialysis or in that used to monitor locomotor activity. After a 4-day or a 1-month withdrawal period, all experiments were performed as described below (Supplementary Figure 1a).

To test the effects of prazosin and SR46349B on the development of neurochemical and behavioral sensitization to MDMA, as well as on the MDMA-induced desensitization of α2A-adrenergic and 5-HT1A autoreceptors function, mice were given a pretreatment (saline or prazosin plus SR46349B) every day 30 min before the injection of MDMA.


Mice were anesthetized with sodium pentobarbital (60 mg kg−1; Sanofi Santé Animale, Libourne, France) and placed in a stereotaxic frame (Kopf Instruments, Tujunga, CA, USA).

An unilateral permanent cannula (CMA/7; CMA Microdialysis, Solna, Sweden) was placed at the edge of the PFC, the LC or the DRN and secured on the skull with screws and dental cement. The coordinates for the guide cannula tip were as follows: PFC—anteroposterior, +2.

6 relative to bregma, mediolateral, +0.5 and dorsoventral, 0 mm from dura; LC—anteroposterior, −5.4 relative to bregma, mediolateral, +0.75 and dorsoventral, −2.4 mm from dura; and DRN—anteroposterior, −4.36 relative to bregma, mediolateral, 0, and dorsoventral, −1.

5 mm from dura, according to the atlas of Paxinos and Franklin32 (Supplementary Figure 1b). After surgery, mice were allowed to recover for at least 4 days.

Monitoring of cortical extracellular monoamines levels

On the day of the experiment, the microdialysis probe was inserted into the PFC (membrane length, 2 mm; diameter, 0.24 mm; cutoff, 6000 Da; CMA/7; CMA Microdialysis), the LC or the DRN (membrane length, 1 mm). Artificial cerebrospinal fluid (in mM: 147 NaCl, 3.5 KCl, 1 CaCl2, 1.2 MgCl2, 1 NaH2PO4, 25 NaHCO3, pH 7.

6) was perfused through the probe at a rate of 1 μl min−1 by a CMA/100 microinjection pump and samples from the PFC were collected in a refrigerated computer-controlled fraction collector (CMA/170). Adequate steady-state monoamines levels in perfusate samples were reached 140 min after probe insertion.

Cortical samples (20 μl every 20 min) were collected for 100 min, to determine basal extracellular values. Then, MDMA, amphetamine, PCA, dexmedetomidine or F13640 were injected either intraperitoneally or infused locally into the PFC, the LC or the DRN through the dialysis probe and cortical samples were collected for 200 min.

In local experiments, the concentration of dexmedetomidine and F13640 was gradually increased every 40 min (i.e. every two samples).


Dialysate samples (20 μl) were injected every 30 min through a rheodyne valve in the mobile phase circuit with a refrigerated automatic injector (Triathlon; Spark Holland, Emmen, The Netherlands). High-performance liquid chromatography was performed with a reverse-phase column (80 × 4.6 mm; 3 μm particle size; HR-80; ESA, Chelmsford, MA, USA).

The mobile phase (for NE analysis: 0.1 M NaH2PO4, 0.1 mM EDTA, 2.75 mM octane sulfonic acid, 0.25 mM triethylamine, 3% methanol, pH 2.9; for 5-HT analysis: 0.1 M NaH2PO4, 0.1 mM EDTA, 2.75 mM octane sulfonic acid, 0.25 mM triethylamine, 15% methanol, 5% acetonitrile, pH 2.9; and for DA analysis: 0.1 M NaH2PO4, 0.1 mM EDTA, 2.

75 mM octane sulfonic acid, 0.25 mM triethylamine, 6% methanol, pH 2.9) was delivered at 0.7 ml min−1 by an ESA-580 pump. An ESA coulometric detector (Coulochem II 5100A, with a 5014B analytical cell; Eurosep Instruments, Cergy, France) was used for electrochemical detection. The conditioning electrode was set at –0.

175 mV and the detecting electrode was set at +0.175 mV.


At the end of the experiment, a blue dye was infused through the microdialysis probe. Then, the brain was quickly removed and immediately frozen at −30 °C using isopentane cooled by dry ice and serial coronal slices were cut on a microtome to ensure the accurate probe implantation.

Locomotor activity

Mice were introduced into a circular corridor (4.5 cm width, 17 cm external diameter) crossed by four infrared beams (1.5 cm above the base) placed at every 90° (Imetronic, Pessac, France).

Locomotor activity was scored when animals interrupted two successive beams and thus had traveled one-quarter of the circular corridor.

Spontaneous activity was recorded for 120 min (habituation to the experimental procedure), and then mice were injected with amphetamine or PCA, and locomotor responses were recorded for an additional 200 min.

Dexmedetomidine-induced sedation

Mice were injected with dexmedetomidine (0.1–0.5 mg kg−1, intraperitoenally) and gently rolled onto their backs 30 min later.

The hypnotic response to dexmedetomidine was defined as the loss of the mouse’s righting reflex (LORR).

The sleep time was measured as the time from the mouse’s inability to right itself when placed on its back until the time when it spontaneously and completely reverted to the prone position.

F13640-induced hypothermia

Body temperature was measured by inserting a 2-cm-long 2-mm-diameter thermistor probe into the rectum of mice that had been gently handled for 20 s. Measurements were made every 10 min for 30 min (basal temperature). Then, the response to a systemic injection of F13640 (0.1–0.

6 mg kg−1, intraperitoneally) was assessed every 10 min until the temperature had returned to the basal value.

For each animal, the hypothermic response to F13640 was calculated as the difference between basal body temperature (calculated as the average temperature during the period before injection) and the minimal body temperature after injection.

Mice were killed by decapitation

The brain was quickly removed and immediately frozen at −30 °C using isopentane cooled by dry ice. Sections (16 μm thick) were cut at −20 °C in a cryostat (Leica CM3050 S, Leica Microsystems, Wetzlar, Germany), and stored at −80 °C for


Effects of Ecstasy (MDMA) on the Brain in Abstinent Users: Initial Observations with Diffusion and Perfusion MR Imaging

The Effects of Ecstasy or MDMA on the Brain

HomeRadiologyVol. 220, No. 3 Neuroradiology

Author Affiliations

  • 1From the Graduate School of Neurosciences, Departments of Nuclear Medicine (L.R., J.B.A.H.) and Radiology (L.R., C.B.L.M.M., J.B.A.H., G.J.d.H.

    ), Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, the Netherlands. Received September 29, 2000; revision requested November 22; revision received January 31, 2001; accepted March 9.

    Address correspondence to L.R. (e-mail: [email protected]).

Published Online:Sep 1 2001


PURPOSE: To evaluate the effects of 3,4-methylenedioxymethamphetamine (MDMA, ecstasy) on the human brain by using diffusion and perfusion magnetic resonance (MR) imaging.

MATERIALS AND METHODS: Eight abstinent ecstasy users and six ecstasy nonusers underwent diffusion and perfusion MR imaging. Apparent diffusion coefficient and relative cerebral volume maps were reconstructed.

Differences in apparent diffusion coefficient values and relative cerebral volume ratios between the groups were analyzed with the Mann-Whitney-Wilcoxon test.

The relationship between apparent diffusion coefficient and relative cerebral volume and the extent of previous ecstasy use was investigated with Spearman rank correlation.

RESULTS: Apparent diffusion coefficient values (0.84 vs 0.65 × 10−5 cm2/sec, P< .025) and relative cerebral volume ratios (1.22 vs 1.01, P< .

025) were significantly higher in the globus pallidus of ecstasy users compared with nonusers, respectively.

Increases in pallidal relative cerebral volume were positively correlated with the extent of previous use of ecstasy (ρ = 0.73, P< .04).

CONCLUSION: Ecstasy use is associated with tissue changes in the globus pallidus. These findings are in agreement with findings in case reports, suggesting that the globus pallidus is particularly sensitive to the effects of ecstasy.


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Published in print: Sept 2001


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