From PsychonautWiki
Jump to: navigation, search
Summary sheet: MDMA
Chemical Nomenclature
Common names MDMA, Molly, Mandy, Emma, MD, Ecstasy, E, X, XTC, Rolls
Substitutive name 3,4-Methylenedioxy-N-methylamphetamine
Systematic name (RS)-1-(Benzo[d][1,3]dioxol-5-yl)-N-methylpropan-2-amine
Class Membership
Psychoactive class Stimulant / Entactogen
Chemical class Amphetamine
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.

Threshold 40 mg
Light 40 - 70 mg
Common 70 - 140 mg
Strong 140 - 180 mg
Heavy 180 mg +
Total 3 - 6 hours
Onset 30 - 45 minutes
Come up 20 - 60 minutes
Peak 1.5 - 2.5 hours
Offset 1 - 1.5 hours
After effects 12 - 48 hours

DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.

3,4-Methylenedioxymethamphetamine (also known as ecstasy, E, XTC, molly, mandy, and MDMA) is an entactogen substance of the phenethylamine class. MDMA is considered to be the prototype member of a group that includes substances like MDA, methylone, and 6-APB, which act by promoting the activity of neurotransmitters serotonin, dopamine, and norepinephrine in the brain.

MDMA was first synthesized in 1912. It first saw use in underground psychotherapy circles in the 1970s.[1] In the 1980s, MDMA spread into nightlife and rave culture and was subsequently banned.[2] In 2014, MDMA was estimated to be one of the most popular recreational drugs used in the world, alongside cocaine and cannabis.[3] Researchers are investigating whether MDMA may assist in treatment-resistant posttraumatic stress disorder (PTSD), social anxiety in autistic adults,[4] and anxiety in those with life-threatening illness.[5][6][7]

Typical effects of MDMA include anxiety relief, disinhibition, enhanced empathy and sociability, relaxation, and euphoria. MDMA is classified as an entactogen due to how it facilitates feelings of closeness with oneself and others. It is commonly associated with dance parties, raves, and electronic dance music.[8] Tolerance to MDMA builds unusually quickly and many users report that it dramatically loses its effectiveness if used on a regular basis. It is commonly recommended to wait one to three months between uses to give the brain enough time to restore serotonin levels.

Acute adverse effects of MDMA are usually the result of high or multiple doses, although single dose toxicity can occur in susceptible individuals.[9] The most serious short-term physical health risks of MDMA are overheating and dehydration, which has resulted in deaths.[10] MDMA has also been shown to be neurotoxic at high doses.[11] However, it is unclear if this risk applies to typical users.[12] It is highly advised to use harm reduction practices if using this substance.

History and culture

MDMA was originally synthesized in 1912 by the Merck chemist Anton Köllisch. Köllisch was interested in developing substances that would help manage excess bleeding and was interested in the activity of MDMA, an intermediary in the production of hydrastinine, a hemostatic agent used at the time. In 1965, Alexander Shulgin synthesized MDMA while conducting experiments with methylenedioxy-substituted compounds but did not test the psychoactivity of the compound.[citation needed]

Around 1975, Shulgin heard about the effects of MDMA from a student. After hearing several more stories about the self-administration of MDMA, he decided to experiment with it. Shulgin was impressed with the effects of the substance and thought it could have therapeutic applications. Shulgin advertised the substance to therapists and psychiatrists for medical use, and it eventually became quite popular in the medical world for the treatment of various psychiatric disorders.[citation needed] During this time, the psychotherapist Dr. Leo Zeff came out of retirement and subsequently introduced the then-legal MDMA to over 4,000 patients. Then known as "Adam", from the mid-1970s to the mid-1980s there was a growth of clinicians using MDMA around California.[13]

The recreational use of MDMA became popular at around the same time, particularly in nightclubs, and eventually caught the attention of the Drug Enforcement Administration. After several hearings, a US Federal Administrative Law Judge recommended that MDMA should be made a Schedule III controlled substance so that it could be used in the medical field. Despite this, the director of the DEA overruled this and classified MDMA as a Schedule I controlled substance.[citation needed]

In the United Kingdom, the 1971 Misuse of Drugs Act, which had already been altered in 1977 to include all ring-substituted amphetamines like MDMA, was further amended in 1985 to refer specifically to Ecstasy, placing it in the Class A category.[13]


MDMA, or 3,4-methylenedioxy-N-methylamphetamine, is a synthetic molecule of the substituted amphetamine class. Molecules of the amphetamine class all contain a phenethylamine core comprised of a phenyl ring bound to an amino (NH2) group through an ethyl chain, with an additional methyl substitution at Rα. In addition to this, MDMA contains a methyl substitution on RN, a feature it shares with methamphetamine. Critically, the MDMA molecule also contains substitutions at R3 and R4 of the phenyl ring with oxygen groups -- these oxygen groups are incorporated into a methylenedioxy ring through a methylene bridge. MDMA shares this methylenedioxy ring with other entactogens and stimulants like MDA, MDEA and MDAI.

Generic structure of a phenethylamine molecule


MDMA acts primarily as a releasing agent of the three principal monoamine neurotransmitters serotonin, norepinephrine, and dopamine through its action at trace amine-associated receptor 1 (TAAR1) and vesicular monoamine transporter 2 (VMAT2).[14][15][16] MDMA is a monoamine transporter substrate (i.e. a substrate for the transporters for dopamine (DAT), norepinephrine (NET), and serotonin (SERT), enabling it to enter monoaminergic neurons via these neuronal membrane transport proteins.[15] By acting as a monoamine transporter substrate, MDMA produces competitive reuptake inhibition at the neuronal membrane transporters, competing for endogenous monoamines for reuptake.[15][17]

MDMA inhibits both vesicular monoamine transporters (VMATs), the second of which (VMAT2) is highly expressed within monoamine neurons vesicular membranes.[16] Once inside a monoamine neuron, MDMA acts as a VMAT2 inhibitor and a TAAR1 agonist.[15][18] The inhibition of VMAT2 by MDMA results in increased concentrations of the aforementioned monoamine neurotransmitters in the cytosol of the neuron.[16][19] Activation of TAAR1 by MDMA triggers protein kinase signaling events which then phosphorylates the associated monoamine transporters of the neuron.[15]

Subsequently, these phosphorylated monoamine transporters either reverse transport direction – i.e. move neurotransmitters from inside the cell to the synaptic cleft – or withdraw into the neuron, respectively producing the inflow of neurotransmitters and noncompetitive reuptake inhibition at the neuronal membrane transporters.[15] MDMA has ten times more affinity for uptake at serotonin transporters compared to dopamine and norepinephrine transporters and consequently has mainly serotonergic effects.[20]

MDMA also has weak agonist activity at postsynaptic serotonin receptors 5-HT1 and 5-HT2 receptors, and its more efficacious metabolite MDA likely augments this action.[21][22][23][24] Cortisol, prolactin, and oxytocin quantities in serum are increased by MDMA.[25]

Additionally, MDMA is a ligand at both sigma receptor subtypes, though its efficacies at these receptors and the role that they play have yet to be elucidated.[26]

Subjective effects

The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. These effects should be taken with a grain of salt and will rarely (if ever) occur all at once, but heavier doses will increase the chances of inducing a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include serious injury or death.

Physical effects

Visual effects

Cognitive effects

Auditory effects

Transpersonal effects

After effects
Aftereffects (3).svg

Experience reports

Anecdotal reports which describe the effects of this compound within our experience index include:

Additional experience reports can be found here:


MDMA Pills, commonly called Ecstasy
Off-white MDMA crystals, commonly called Molly

Since the 1980s, MDMA has become widely known as "Ecstasy" (shortened to "E", "X", or "XTC"), usually referring to its street forms as illicitly pressed pills or tablets.[40] The American term "Molly" and the British equivalent term "Mandy" originally referred to crystal or powder MDMA that was purported to be of high purity and free of adulteration.[41] However, it has since evolved into a generic street term for any number of euphoric stimulants that are sold in powder or crystal form.[citation needed]

MDMA can be found in a number of forms:

  • Pills are the most common form in which MDMA is sold, and are commonly referred to as Ecstasy. They often contain other substances or adulterants that range from anything from MDA, MDEA, amphetamine, methamphetamine, caffeine, 2C-B or mCPP to synthesis by-products such as MDP2P, MDDM or 2C-H. They can also contain an array random substances such as research chemicals, prescription drugs, over-the-counter drugs, poisons or nothing at all. It is strongly recommended to take harm reduction measures such as using a reagent testing kit when ingesting unknown pills.
  • Crystals or Powder (commonly called Molly) is a white to brownish substance which can be dissolved, crushed, put into gel capsules or edible paper ("parachutes"). It can be administered orally, sublingually, buccally or via insufflation ("snorting" or "sniffing").


MDMA-assisted psychotherapy for PTSD

In 2011, a pilot study on 20 patients demonstrated promising results in the treatment of post-traumatic stress disorder (PTSD). After two or three MDMA-assisted psychotherapy sessions, 83% of the patients no longer met the criteria for PTSD, compared to only 25% in the control group where MDMA was replaced with a placebo. The results sustained at two and twelve months after the treatment. The MDMA and placebo group both received non-drug psychotherapy before and after the sessions. In the study, a dose of 125mg MDMA plus a 62.5mg supplemental dose after 2 hours have been administered.[42] After completion of the study, the patients from the placebo group also received MDMA-assisted psychotherapy, and a long-term follow-up study of 19 patients published in 2013 shows that even after three years the positive results maintained.[43]

In 2017, the FDA granted MDMA a breakthrough therapy designation for PTSD, meaning if studies show promise, a review for potential medical use could occur more quickly.[44] Phase 3 clinical trials to look at effectiveness and safety expected to begin in 2018.[45]


MDMA is typically produced and consumed in its racemic form (known as SR-MDMA) which consists of equal parts S-MDMA and R-MDMA. A 2017 study found that high doses of R-MDMA administered in mice increased prosocial behavior and facilitated fear-extinction learning but did not produce hyperthermia or signs of neurotoxicity. This is thought to owe itself to the lower dopamine release R-MDMA displays relative to SR-MDMA. This result suggests that R-MDMA may be a safer and more viable therapeutic than racemic MDMA.[46]

Toxicity and harm potential

Radar plot showing relative physical harm, social harm, and dependence of MDMA[47]

The short-term physical health risks of MDMA consumption include dehydration, insomnia, hyperthermia,[48][49] and hyponatremia.[50] Continuous activity without sufficient rest or rehydration may cause body temperature to rise to dangerous levels, and loss of fluid via excessive perspiration puts the body at further risk as the stimulatory and euphoric qualities of the drug may render the user oblivious to their energy expenditure for quite some time. Diuretics such as alcohol may exacerbate these risks further due to the excessive amounts of dehydration they may cause.

The exact toxic dosage is unknown, but considered to be far greater than its effective dose.[citation needed]


The neurotoxicity of MDMA use has long been the subject of debate. Scientific study has resulted in the general agreement that, although it is physically safe to try in a responsible context, the administration of repeated or high dosages of MDMA is most certainly neurotoxic in some form.

Administration of MDMA causes subsequent down-regulation of serotonin reuptake transporters in the brain. The rate at which the brain recovers from serotonergic changes is unclear. One study demonstrated lasting serotonergic changes in some animals exposed to MDMA.[51] Other studies have suggested that the brain may recover from serotonergic damage.[52][53][54]

It is thought that MDMA's metabolites play a large role in the in the uncertain levels of neurotoxicity. For example, a metabolite of MDMA called alpha-MethylDopamine (which is known to be toxic to dopamine neurons[55][56]) was thought believed to be involved in the toxicity of MDMA to serotonin receptors. However, one study found this to not be the case as direct administration of aMD did not cause neurotoxicity.[56] Additionally, MDMA injected directly into the brain was found to not be toxic, implying a metabolite is responsible for the toxicity when MDMA is administered via insufflation or oral consumption.[56]

This study found that although aMD is involved, it is a further metabolite of aMD involving glutathione that is primarily responsible for the selective damage to 5-HT receptors triggered by MDMA/MDA.[56]This metabolite forms in higher concentrations when core temperature is elevated. It is taken up into serotonin receptors by its transporters and metabolized by MAO-B into a reactive oxygen species which can cause neurological damage.[56][57]


The long-term heavy use of MDMA has been shown to be cardiotoxic and may lead to valvulopathy (heart valve damage) through its actions on the 5-HT2B receptor.[58][59] In one study, 28% of long-term users (2-3 doses per week for a mean of 6 years, mean of age 24.3 years) had developed clinically evident valvular heart disease.[60]

It is strongly recommended that one use harm reduction practices when using this substance.

Tolerance and addiction potential

As with other stimulants, the chronic use of MDMA can be considered moderately addictive with a high potential for abuse and is capable of causing psychological dependence among certain users. When addiction has developed, cravings and withdrawal effects may occur if one suddenly stops their usage.

Tolerance to many of the effects of MDMA develops with prolonged and repeated use. This results in users having to administer increasingly larger doses to achieve the same effects. Upon a single administration, it takes about 1 month for the tolerance to be reduced to half and 2.5 months to be back at baseline (in the absence of further consumption). MDMA presents cross-tolerance with all dopaminergic and serotonergic stimulants, meaning that after the consumption of MDMA all stimulants will have a reduced effect.

Dangerous interactions

Although many psychoactive substances are safe to use on their own, they can quickly become dangerous or even life-threatening when combined with other substances. The following lists some known dangerous combinations, but may not include all of them. A combination that appears to be safe in low doses can still increase the risk of injury or death. Independent research should always be conducted to ensure that a combination of two or more substances is safe to consume.

  • MDMA - The neurotoxic effects of MDMA may be increased when combined with other amphetamines.
  • Cocaine - This combination may increase strain on the heart.
  • Stimulants - MDMA can be potentially dangerous in combination with other stimulants as it can increase one's heart rate and blood pressure to dangerous levels.
  • 25x-NBOMe & 25x-NBOH - Members of the 25x family are highly stimulating and physically straining. Combinations with stimulants should be avoided due to the risk of excessive stimulation. This can result in panic attacks, thought loops, seizures, increased blood pressure, vasoconstriction, and heart failure in extreme cases.
  • Alcohol - Alcohol can be dangerous to combine with stimulants due to the risk of accidental over-intoxication. Stimulants mask the sedative effects of alcohol, which is the main factor people use to assess their degree of intoxication. Once the stimulant wears off, the depressant effects of alcohol are left unopposed, which can result in blackouts and respiratory depression. If combined, one should strictly limit themselves to only drinking a certain amount of alcohol per hour.
  • DXM - Combinations with DXM should be strictly avoided due to DXM's effects on serotonin and dopamine reuptake. This can lead to panic attacks, hypertensive crisis, or serotonin syndrome.
  • MXE - Combinations with MXE may dangerously elevate blood pressure and increase the risk of psychosis.
  • Tramadol - Tramadol lowers the seizure threshold.[61] Combinations with stimulants may further increase this risk.
  • Stimulants - The neurotoxic and cardiotoxic effects of MDMA may be increased when combined with other stimulants.
  • Cocaine - This combination may increase strain on the heart to dangerous levels.
  • Psychedelics - There is some evidence that the combination of MDMA and serotonergic psychedelics may increase the neurotoxicity of MDMA. [62][63][64]

Serotonin syndrome risk

Combinations with the following substances can cause dangerously high serotonin levels. Serotonin syndrome requires immediate medical attention and can be fatal if left untreated.

There is an increased risk of serotonin syndrome when MDMA is taken with many antidepressants, particularly selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs). Additionally, if MDMA is taken with SSRIs and SNRIs, it will be significantly less active or may not produce any distinguishable effects at all.[citation needed]

Legal status

  • Austria: MDMA is illegal to possess, produce and sell under the SMG (Suchtmittelgesetz Österreich).[citation needed]
  • Belgium: MDMA is illegal to possess, produce and sell in Belgium.[citation needed]
  • Brazil: MDMA is illegal to possess, produce and sell in Brazil.[citation needed]
  • Canada: MDMA is a Schedule I drug in Canada.[66]
  • Denmark: MDMA is illegal to possess, produce and sell in Denmark.[citation needed]
  • Egypt: MDMA is a Schedule III drug in Egypt.[citation needed]
  • Finland: MDMA is illegal to possess, produce and sell in Finland.[citation needed]
  • Germany: MDMA is an Anlage I controlled drug in Germany.[citation needed]
  • Latvia: MDMA is a Schedule I drug in Latvia.[67]
  • The Netherlands: MDMA is illegal to possess, produce and sell in the Netherlands.[citation needed]
  • New Zealand: MDMA is a Class B1 drug in New Zealand.[citation needed]
  • Norway: MDMA is illegal to possess, produce and sell in Norway.[citation needed]
  • Sweden: MDMA is illegal to possess, produce and sell in Sweden.[citation needed]
  • Switzerland: MDMA is illegal to possess, produce and sell in Switzerland.[citation needed]
  • United Kingdom: MDMA is a Class A drug in the UK.[citation needed]
  • United States: MDMA is a Schedule I drug in the US.[citation needed]

See also

External links



  1. Ann Shulgin; Alexander Shulgin (1991). PiHKAL: A Chemical Love Story. Part I. Chapter 12. Transform Press.
  2. Pharmaceutical company unravels drug's chequered past |
  3. Global drug survey: 2014. |
  4. ClinicalTrials. (n.d.). MDMA-assisted Therapy for Social Anxiety in Autistic Adults - Full Text View - Retrieved from
  5. Multidisciplinary Association for Psychedelic Studies. (n.d.). MAPS - MDMA-Assisted Psychotherapy for Anxiety Associated with Life-Threatening Illness. Retrieved from
  6. 3,4-methylenedioxymethamphetamine (MDMA): current perspectives - Jerrold S Meyer |
  7. The potential dangers of using MDMA for psychotherapy - Parrott AC |
  8. World Health Organization (2004). Neuroscience of Psychoactive Substance Use and Dependence. World Health Organization. pp. 97–. ISBN 978-92-4-156235-5. Archived from the original on 28 April 2016.
  9. Meyer JS (2013). "3,4-methylenedioxymethamphetamine (MDMA): current perspectives". Subst Abuse Rehabil. 4: 83–99. doi:10.2147/SAR.S37258. PMC 3931692 Freely accessible. PMID 24648791.
  10. Greene SL, Kerr F, Braitberg G (October 2008). "Review article: amphetamines and related drugs of abuse". Emerg. Med. Australas. 20 (5): 391–402. doi:10.1111/j.1742-6723.2008.01114.x. PMID 18973636
  11. Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. p. 375. ISBN 9780071481274.
  12. Gouzoulis-Mayfrank, E; Daumann, J (2009). "Neurotoxicity of drugs of abuse—the case of methylenedioxyamphetamines (MDMA, ecstasy), and amphetamines". Dialogues Clin Neurosci. 11 (3): 305–17. PMC 3181923 Freely accessible. PMID 19877498.
  13. 13.0 13.1 Sessa, B. (2017). The experience and the drugs. In The Psychedelic Renaissance: Reassessing the Role of Psychedelic Drugs in 21st Century Psychiatry and Society (2nd ed., p. 60). London: Muswell Hill Press.
  14. "3,4-Methylenedioxymethamphetamine". 'Hazardous Substances Data Bank. National Library of Medicine. 28 August 2008. Retrieved 22 August 2014.
  15. 15.0 15.1 15.2 15.3 15.4 15.5 Miller, G. M. (2011). The emerging role of trace amine‐associated receptor 1 in the functional regulation of monoamine transporters and dopaminergic activity. Journal of Neurochemistry, 116(2), 164-176. https://doi.10.1111/j.1471-4159.2010.07109.x
  16. 16.0 16.1 16.2 Eiden LE, Weihe E. VMAT2: a dynamic regulator of brain monoaminergic neuronal function interacting with drugs of abuse. Ann. N. Y. Acad. Sci. 1216(1)1. 86–98. January 2011.
  17. Fitzgerald JL, Reid JJ. Effects of methylenedioxymethamphetamine on the release of monoamines from rat brain slices. European Journal of Pharmacology. 191(2). 217–20. 1990.}}
  18. Eiden LE, Weihe E (January 2011). "VMAT2: a dynamic regulator of brain monoaminergic neuronal function interacting with drugs of abuse". Ann. N. Y. Acad. Sci. 1216 (1): 86–98.
  19. Bogen IL, Haug KH, Myhre O, Fonnum F. Short- and long-term effects of MDMA ("ecstasy") on synaptosomal and vesicular uptake of neurotransmitters in vitro and ex vivo. Neurochemistry International. 43. 4–5. 393–400. 2003
  20. Nelson, Lewis S.; Lewin, Neal A.; Howland, Mary Ann; Hoffman, Robert S.; Goldfrank, Lewis R.; Flomenbaum, Neal E. (2011). Goldfrank's toxicologic emergencies (9th ed.). New York: McGraw-Hill Medical. ISBN 978-0071605939.
  21. Battaglia G, Brooks BP, Kulsakdinun C, De Souza EB. Pharmacologic profile of MDMA (3,4-methylenedioxymethamphetamine) at various brain recognition sites.European Journal of Pharmacology. 149(1–2)1. 59–63. (1988).
  22. Lyon RA, Glennon RA, Titeler M . (1986) 3,4-Methylenedioxymethamphetamine (MDMA): stereoselective interactions at brain 5-HT1 and 5-HT2 receptors. Psychopharmacology. 88(4). 525–6.
  23. Nash JF, Roth BL, Brodkin JD, Nichols DE, Gudelsky GA. Effect of the R(-) and S(+) isomers of MDA and MDMA on phosphatidylinositol turnover in cultured cells expressing 5-HT2A or 5-HT2C receptors. Neuroscience Letters. 177(1–2). 111–5 . (1994). https//
  24. Setola V, Hufeisen SJ, Grande-Allen KJ, Vesely I, Glennon RA, Blough B, Rothman RB, Roth BL. 3,4-methylenedioxymethamphetamine (MDMA, "Ecstasy") induces fenfluramine-like proliferative actions on human cardiac valvular interstitial cells in vitro. Molecular Pharmacology. 63(6). 1223–9 (2003).
  25. Betzler, Felix; Viohl, Leonard; Romanczuk-Seiferth, Nina; Foxe, John (January 2017). "Decision-making in chronic ecstasy users: a systematic review." European Journal of Neuroscience. 45 (1): 34–44. https://doi:10.1111/ejn.13480...the addictive potential of MDMA itself is relatively small.
  26. Matsumoto RR. Targeting Sigma Receptors: Novel Medication Development for Drug Abuse and Addiction. Expert Rev Clin Pharmacology. 2(4), 351–8. July 2009.
  27. The pharmacology and toxicology of “ecstasy” (MDMA) and related drugs |
  28. Effects of MDMA, MDA and MDEA on blood pressure, heart rate, locomotor activity and body temperature in the rat involve a-adrenoceptors - Sotiria Bexis & James R. Docherty |
  29. The pharmacology and toxicology of “ecstasy” (MDMA) and related drugs |
  30. Effects of MDMA on body temperature in humans - Matthias E Liechti |
  31. 3,4-Methylenedioxymethamphetamine (MDMA, Ecstasy) and Driving Impairment - Logan, BK & Couper, FJ |
  32. Brvar M, Kozelj G, Osredkar J, Mozina M, Gricar M, Bunc M. Polydipsia as another mechanism of hyponatremia after 'ecstasy' (3,4 methyldioxymethamphetamine) ingestion. Eur J Emerg Med. 2004 Oct;11(5):302-4. |
  33. Bora F, Yılmaz F, Bora T. Ecstasy (MDMA) and its effects on kidneys and their treatment: a review. Iranian Journal of Basic Medical Sciences. 2016;19(11):1151-1158. |
  34. Inman, D. S., & Greene, D. (2003). ‘The agony and the ecstasy’: acute urinary retention after MDMA abuse. BJU international, 91(1), 123-123.
  36. A method of conducting therapeutic sessions with MDMA. - Greer GR, Tolbert R. |
  38. Bruxism after 3,4-methylenedioxymethamphetamine (ecstasy) abuse - Bruxism and ecstasy Ricardo Jorge Dinis-Oliveira et al. |
  39. Urban Dictionary page on "gurning"
  40. The Pharmacology and Clinical Pharmacology of 3,4-Methylenedioxymethamphetamine (MDMA, “Ecstasy”) - A. Richard Green et al. |
  41. 3 cases of primary intracranial hemorrhage associated with “Molly”, a purified form of 3,4-methylenedioxymethamphetamine (MDMA) |
  42. Mithoefer, Michael C., et al. “Durability of Improvement in Post-Traumatic Stress Disorder Symptoms and Absence of Harmful Effects or Drug Dependency after 3,4-Methylenedioxymethamphetamine-Assisted Psychotherapy: A Prospective Long-Term Follow-up Study.” Journal of Psychopharmacology (Oxford, England) 27.1 (2013): 28–39. 10.1177/0269881112456611
  43. Mithoefer, Michael C., et al. “Durability of Improvement in Post-Traumatic Stress Disorder Symptoms and Absence of Harmful Effects or Drug Dependency after 3,4-Methylenedioxymethamphetamine-Assisted Psychotherapy: A Prospective Long-Term Follow-up Study.” Journal of Psychopharmacology (Oxford, England) 27.1 (2013): 28–39.
  44. Wan, William (26 August 2017). "Ecstasy could be 'breakthrough' therapy for soldiers, others suffering from PTSD". Washington Post. Archived from the original on 29 August 2017. Retrieved 29 August 2017.
  45. Feduccia, AA; Holland, J; Mithoefer, MC (February 2018). "Progress and promise for the MDMA drug development program". Psychopharmacology. 235 (2): 561–571. doi:10.1007/s00213-017-4779-2. PMID 29152674.
  46. Curry, D. W., Young, M. B., Tran, A. N., Daoud, G. E., & Howell, L. L. (2018). Separating the agony from ecstasy: R (–)-3, 4-methylenedioxymethamphetamine has prosocial and therapeutic-like effects without signs of neurotoxicity in mice. Neuropharmacology, 128, 196-206.
  47. Nutt, D., King, L. A., Saulsbury, W., & Blakemore, C. (2007). Development of a Rational Scale to Assess the Harm of Drugs of Potential Misuse, 1047–1053.
  48. Nimmo, S. M., Kennedy, B. W., Tullett, W. M., Blyth, A. S., & Dougall, J. R. (1993). Drug‐induced hyperthermia. Anaesthesia, 48(10), 892-895.
  49. Malberg, J. E., & Seiden, L. S. (1998). Small changes in ambient temperature cause large changes in 3, 4-methylenedioxymethamphetamine (MDMA)-induced serotonin neurotoxicity and core body temperature in the rat. Journal of Neuroscience, 18(13), 5086-5094. PMID: 9634574.
  50. Wolff, K., Tsapakis, E. M., Winstock, A. R., Hartley, D., Holt, D., Forsling, M. L., & Aitchison, K. J. (2006). Vasopressin and oxytocin secretion in response to the consumption of ecstasy in a clubbing population. Journal of Psychopharmacology, 20(3), 400-410.
  51. Reorganization of ascending 5-HT axon projections in animals previously exposed to the recreational drug (+/-)3,4-methylenedioxymethamphetamine (MDMA, "ecstasy") ( / NCBI) |
  52. Scheffel, U., Szabo, Z., Mathews, W. B., Finley, P. A., Dannals, R. F., Ravert, H. T., ... & Ricaurte, G. A. (1998). In vivo detection of short‐ and long‐term MDMA neurotoxicity—a positron emission tomography study in the living baboon brain. Synapse, 29(2), 183-192.<183::AID-SYN9>3.0.CO;2-3
  53. Reneman, L., Lavalaye, J., Schmand, B., de Wolff, F. A., van den Brink, W., den Heeten, G. J., & Booij, J. (2001). Cortical serotonin transporter density and verbal memory in individuals who stopped using 3, 4-methylenedioxymethamphetamine (MDMA or ecstasy): preliminary findings. Archives of General Psychiatry, 58(10), 901-906. Chicago.
  54. Selvaraj, S., Hoshi, R., Bhagwagar, Z., Murthy, N. V., Hinz, R., Cowen, P., ... & Grasby, P. (2009). Brain serotonin transporter binding in former users of MDMA (‘ecstasy’). The British Journal of Psychiatry, 194(4), 355-359.
  55. Neurotoxic thioether adducts of 3,4-methylenedioxymethamphetamine identified in human urine after ecstasy ingestion ( / NCBI) | |
  56. 56.0 56.1 56.2 56.3 56.4 2,5-Bis-(glutathion-S-yl)-alpha-methyldopamine, a putative metabolite of (+/-)-3,4-methylenedioxyamphetamine, decreases brain serotonin concentrations ( / NCBI) - Miller RT et al. |
  57. Drug-induced Valvulopathy: An Update - Chandikumar S. Elangbam |
  58. Huang, X. P., Setola, V., Yadav, P. N., Allen, J. A., Rogan, S. C., Hanson, B. J., ... & Roth, B. L. (2009). Parallel functional activity profiling reveals valvulopathogens are potent 5-hydroxytryptamine2B receptor agonists: implications for drug safety assessment. Molecular Pharmacology, 76(4), 710-722.
  59. Drug-induced Valvulopathy: An Update - Chandikumar S. Elangbam |
  60. Possible association between 3,4-methylenedioxymethamphetamine abuse and valvular heart disease. ( / NCBI) |
  61. Talaie, H., Panahandeh, R., Fayaznouri, M. R., Asadi, Z., & Abdollahi, M. (2009). Dose-independent occurrence of seizure with tramadol. Journal of Medical Toxicology, 5(2), 63-67.
  62. Armstrong, B. D., Paik, E., Chhith, S., Lelievre, V., Waschek, J. A., & Howard, S. G. (2004). Potentiation of (DL)‐3, 4‐methylenedioxymethamphetamine (MDMA)‐induced toxicity by the serotonin 2A receptior partial agonist d‐lysergic acid diethylamide (LSD), and the protection of same by the serotonin 2A/2C receptor antagonist MDL 11,939. Neuroscience Research Communications, 35(2), 83-95.
  63. Potentiation of MDMA-induced dopamine release and serotonin neurotoxicity by 5-HT2 receptor agonists |
  64. Ecstasy induces apoptosis via 5-HT(2A)-receptor stimulation in cortical neurons. |
  65. Gillman, P. K. (2005). Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity. British Journal of Anaesthesia, 95(4), 434-441.
  66. Canada controlled drugs and substances |
  67. Noteikumi par Latvijā kontrolējamajām narkotiskajām vielām, psihotropajām vielām un prekursoriem (3,4-Metilēndioksifeniletānamīni) |