Thuốc lắc
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  Thuốc lắc - MDMA |
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1-(benzo[d][1,3]dioxol-5-yl)-N-methylpropan-2-amine |
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| Mã CAS |
42542-10-9 |
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| Công thức hóa học | C11H15NO2 |
| Trọng lượng phân tử | 193.25 g/mol |
| Công thức hóa học đơn giản | CC(NC)CC1=CC=C(OCO2)C2=C1 |
| Thời gian bán thải | Dạng "S" khoảng 4 tiếng, dạng "R" gần 14 tiếng |
| Dạng thuốc | Viên uống - 75-120 mg Viên tan dưới lưỡi - 100 mg |
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Thuốc lắc ecstasy, tên khoa học là MethyleneDioxyMethamphetAmine (tắt: MDMA), là một dạng ma tuý tổng hợp (lần đầu tiên năm 1910), và sau đó 2 năm thuộc quyền sở hữu của công ty dược Merck (Đức) dưới dạng chất ức chế cảm giác thèm ăn.
Mục lục |
[sửa] Lịch sử
A patent for MDMA was originally filed on Christmas eve 1912 by the German pharmaceutical company Merck, and granted two years later (to the day). At the time, MDMA was not known to be a drug in its own right; rather, it was patented as an intermediate chemical used in the synthesis of a styptic (a drug intended to control bleeding from wounds.) Over half a century would pass before the first known ingestion of MDMA by humans.
The U.S. Army did, however, do lethal dose studies of it and several other compounds in the mid-1950's. It was given the name EA-1475, with the EA standing for Edgewood Arsenal. The results of these studies were not declassified until 1969. MDMA was first brought to public attention through Dr. Alexander Shulgin in the 1960s who recommended it for use in certain therapy sessions, naming the drug 'window' (he discovered it while searching for compounds that have a similar psychoactive effect as other compounds contained in nutmeg). It was widely used therapeutically by US psychotherapists because of its empathogenic effects until its criminalization in the late 1980s. The drug was hailed as a miracle by therapists and counselors who claimed couples could have six months worth of progress in one use of the drug, and soldiers returning from the Vietnam war could overcome their PTSD sometimes more effectively than talk or group therapy. A small number of therapists used it in their practices until it was made illegal.
Until 1985, MDMA was legal in the United States. Recreationally, it first came into prominence in certain trendy yuppie bars in the Dallas area, then in gay dance clubs. From there, use spread to rave clubs, and then to mainstream society and remains popular to this day. During the 1990s, along with the growing popularity of the rave subculture, MDMA use became increasingly popular among young adults in universities and later in high schools. It rapidly became one of the four most widely used illegal drugs in the US, along with cocaine, heroin and marijuana.
In the late 80's and early 90's ecstasy was widely used in the United Kingdom and other parts of Europe, becoming an integral element of rave culture. It was also associated with another psychedelic/dancefloor-influenced music scene, Madchester.
[sửa] Sự tiêu khiển
Thuốc lắc tạo nên cho người dùng những cảm giác kích thích cao độ. Tác dụng chính là gồm có : thấy tinh thần cởi mở, sảng khoái, thích yêu đương, dễ cảm thông với người chung quanh, nâng cao cảm giác trong cơ thể, và tự tin. Vì những tác dụng này mà thuốc lắc rất phổ biến tại các vũ trường. Dân xài thuốc có cảm tưởng mình gần giống như ... siêu nhân, có thể nhảy nhót nhiều và lâu hơn, ăn nói hoạt bát hơn, thích thú hơn và nhạc có vẻ hay hơn. Những người hay mắc cở, thiếu tự tin khi xài thuốc sẽ có cảm tưởng mình được đổi thành người tự tin, hoạt bát hơn.
[sửa] Sự cung cấp và quản lý
MDMA is usually ingested in pill form. Pills come in a variety of "brands", usually identified by the icons stamped on the pills. The brands never consistently designate the actual active compound within the pill, as anyone can make their own pills which copy the features of a well-known brand.
Pills sold illegally on the street don't always have MDMA as the only active ingredient. There is a widely held belief that black market pills usually contain methamphetamine, although analysis of police seizures show this is only rarely true in most areas [cần chú thích]. In British Columbia, Canada, however, recent government tests showed that some of the pills tested contained Methamphetamine in doses as high as 20 milligrams [cần chú thích]. Analogues of MDMA such as MDEA, MDA and MBDB are often found, and more rarely other psychoactive additives such as amphetamines (speed), DXM, ephedrine, Pseudophedrine, PMA, 4-MTA, caffeine, ketamine (Special K), 2C-B, 2C-T-7 or other compounds may be present [cần chú thích]. In addition to MDMA ecstasy pills may contain cocaine, heroin, or mescaline [cần chú thích]; Mescaline is an especially unlikely contaminant, as a large amount is required for an effective dose [cần chú thích]. There have been a few cases where an extremely potent synthetic opiate, Fentanyl, has been identified in pills [cần chú thích], which could potentially be very dangerous if people took several of them thinking that they only contained MDMA [cần chú thích].
Aspirin, paracetamol (acetaminophen), or even canine heartworm tablets have had the letter E scratched into them and have been sold as ecstasy [cần chú thích], for enormous profit. While overdose from MDMA itself is rare, many more toxic substances are often sold as ecstasy [cần chú thích], and overdose or other adverse reaction to adulterants is not uncommon [cần chú thích].
Although full and proper characterization of ecstasy pills requires advanced lab techniques such as Gas chromatography-mass spectrometry, it is also possible to use a less accurate presumptive alkaloid test known as the Marquis reagent. DanceSafe sells testing kits, and includes an extensive database of photographs of different pills, along with the results of a laboratory analysis of their contents. EcstasyData.org [1] is a non-profit site that tests the purity of street pills and compiles results. Most blackmarket pills are made in basement labs with household chemicals [cần chú thích](often containing other products) and are thus dangerous because of their impure content.
[sửa] Hiệu ứng, tác dụng
[sửa] Hiệu ứng của thuốc mà người dùng mong muốn
[sửa] Tác dụng tới cơ thể
[sửa] Những ảo giác tức thời
MDMA is metabolised via three pathways. One such pathway proceeds via N-demethylation, byproducts of which include several active metabolites, including MDA. The metabolism is primarily by the cytochrome P450 enzymes CYP2D6 (in humans, but CYP2D1 in mice), and CYP3A4. Complex, nonlinear pharmacokinetics arise via autoinhibition of CYP2D6 and CYP2D8, resulting in zeroth order kinetics at higher doses. This can result in sustained and higher drug concentrations if the user takes consecutive doses of the drug. A significant quantity is excreted unchanged in the urine, especially when the drug is taken at higher doses.
Serotonin is a neurotransmitter believed to play a role in the regulation of mood and pleasure. MDMA's main action is believed to cause serotonin vesicles in the neurons to release quantities of serotonin into the synapses. MDMA also has agonist effects on dopamine and norepinephrine, and promotes the release of the hormone prolactin. These effects are primarily due to MDMA's action on the monoamine transporters, SERT (serotonin transporter), DAT (dopamine transporter) and NET (norepinephrine transporter).
[sửa] Hậu quả lâu dài
Long-term effects are still unknown and heavily debated among scientists. There are several reports of Hallucinogen Persisting Perception Disorder being induced by MDMA. In some cases, the disorder appears to be permanent. The disorder seems to occur in only a small fraction of a percentage of users, and its mechanism of causation is unknown.
Some experiments indicate that prolonged or excessive use at very high doses may lead to the synaptic terminals of serotonin neurons being damaged. The precise mechanism of this action is unknown, but recent evidence (Jones 2004; Miller 1997; Monks et al. 2004) suggests that the metabolic breakdown of MDMA includes the formation of reactive oxygen species (ROS), chemicals known to cause oxidative cell damage when taken up into the releasing synapse.
This effect has been experimentally verified in the brains of rats, where the serotonin terminals of animals who are given extremely high doses of MDMA over a prolonged period of time (usually ten to one hundred times greater than a typical human dose) become withered and useless, although this isn't certain[2][3]. This hypothesis is supported by the fact that the administration of selective serotonin reuptake inhibitors ("SSRIs", which bind to the serotonin cell's reuptake transporters and thus block ROS from entering the serotonin cells) along with or immediately following MDMA seems to block neuron damage in rats given MDMA.
The mechanism proposed as a large part of this neurotoxicity and its functional consequences appear to involve the induction of oxidative stress. This stress results from an increase in free radicals and a decrease in antioxidants in the brain. (Shankaran, 2001) Oxidation is part of the normal metabolic processes of the body. As the cell goes about its life, by-products called oxidative radicals are formed, also called free radicals. These molecules have an unpaired electron that makes them highly reactive. They pull strongly on the electrons of neighboring molecules and destabilize the electrical balance of those molecules, sometimes causing those molecules to fall apart. This can become a chain reaction.
In normal functioning, there are antioxidants in the system that act as free radical scavengers. These are molecules with an extra electron that they are willing to give up to the free radicals, making both the free radical and the antioxidant more stable. MDMA rapidly increases the levels of free-radicals in the system and overwhelms the reserves of scavengers. The radicals then damage cell walls, reduce the flexibility of blood vessels, destroy enzymes, and cause other molecular damage in the neurological pathways. (Erowid, 2001) It has been shown that MDMA-neurotoxic effects are increased by a hyperthermic environment and decreased by a hypothermic one. (Yeh, 1997)
Studies have suggested that the neurotoxic molecules are not hydroxyl free radicals, but superoxide free radicals. When rats are injected with salicylate, a molecule that scavenges hydroxyl free radicals, the neurotoxic effects of MDMA are not attenuated, but actually potentiated. Further evidence of this superoxide theory comes from the observation that CuZn-superoxide dismutase transgenic mice (mice with excess human antioxidant enzyme) demonstrate neuroprotective mechanisms that protect the mice from MDMA-induced depletion of 5-HT and 5-HIAA and lethal effects. (Baggott, 2001 and Yeh, 1997)
Studies giving animal species injections have shown that ascorbic acid, alpha lipoic acid, l-cysteine, and some other radical scavengers are effective in reducing oxidative stress caused by MDMA. (Erowid, 2001) A combination of antioxidants, including Vitamin A, C, and E are recommended; taking multivitamins including selenium, riboflavin, zinc, cartenoids, etc. should help reduce oxidative damage. Many of these vitamins, though, are water soluble, and are quickly excreted from the body. The typical MDMA user is psychoactive for 4-6 hours and may not have an appetite from the time of taking until the following sleep cycle or many hours later. These vitamins flush through the system in 3-4 hours. Damage occurs in the absence of these antioxidants.
There are some fallacies in applying these animal studies to human use. First, it’s difficult to equate rat doses to human doses; the rat metabolizes MDMA twice as fast as a human and often larger doses or multiple doses are administered to simulate human plasma levels. The doses given in experiments are far greater than typical human use of 100-300 mg in order to notice the problems caused so that we may say that if this happens at large doses, then a lesser form should happen at low doses. There could be a threshold of nothing happening or a threshold of the worst problems at low doses.
Second, the doses of antioxidants given to these animals are much higher than humans would ever take both in its vehicle (injected vs. oral) and in its dosage. So essentially both the neurotoxic and neuroprotective effects are exaggerated, but we cannot say if this scales down the same way.
Some MDMA users administer an SSRI while, or shortly after taking MDMA, in an attempt to prevent possible neurotoxicity. These SSRIs are typically antidepressants such as fluoxetine or sertraline. However, administration of SSRIs before using MDMA is known to block the euphoric high from the drug, due to the regulation of serotonin. This blocking effect can last several weeks, depending on the half-life of the SSRI. The same effects are seen with recent cocaine use, which itself is an SSRI.
It should be noted, however, that MDMA use in conjunction with a different class of antidepressants, namely Monoamine oxidase inhibitors, is strongly contra-indicated due to danger of serotonin syndrome and the possibility of life-threatening hypertension. The safety of this practice has not been systematically evaluated.
Many users also attempt to replenish the deficit of serotonin which follows the use of MDMA by administering 5-HTP. The serotonin precursor 5-HTP, which is commercially available as a dietary supplement, reportedly supplies the user with more of the raw materials to synthesize the neurotransmitter. Pre-loading with 5-HTP has not been shown to increase the subjective effects of MDMA.
Because MDMA's neurotoxicity is known to be highly dependent on its metabolic disposition (Jones 2004; de la Torre & Farré 2004), it is not known whether experiments in rats and monkeys have any direct bearing on human users.
Considerable research has been done into possible cognitive-behavioral deficits among ecstasy users but data have been largely inconclusive. At least two meta-analyses of these studies have been completed (Morgan 2000; Sumnall & Cole 2005). Morgan's analysis of 17 studies showed that ecstasy users had a slight tendency to be more impulsive and depressed than controls. Sumnall and Cole's analysis showed a slight increase in the prevalence of depressive symptoms in ecstasy users over controls. Of course, in retrospective studies like these we are always faced with a chicken-or-egg question: did these impulsive and depressed people use ecstasy to self-medicate or did otherwise normal people become depressed and impulsive after using ecstasy? This question has not been answered. Moreover, such research is problematic as ecstasy users are much more likely than control subjects to have taken other drugs in addition to ecstasy. This makes it difficult for researchers to establish a direct causal relationship.
Although some experimental evidence exists indicating that long-term ecstasy users experience memory difficulties, a large study in 2002 (Strote et al.) showed that ecstasy users in 4-year colleges have GPAs which do not differ significantly from those of non-users.
According to one study, MDMA use has led to rhabdomyolysis (muscle breakdown) as a consequence of MDMA-induced hyperpyrexia (abnormally high body temperature). Rhabdomyolysis can cause renal failure and death. Note the "degree to which the seriousness of the effects can be dependent on environmental factors other than the drug concentration" in describing the fact that of the fatalities, blood concentrations of the drug spanned a large range. This notwithstanding, "most of the cases of serious toxicity or fatality have involved blood levels... up to 40 times higher than the usual recreational range." (Kalant H., 2001) [1]
[sửa] Thuốc lắc và bệnh Parkinson
Research at the University of Manchester indicates that MDMA dramatically reduces tremors in patients receiving L-DOPA treatment for Parkinson's Disease.
In a now-retracted study, a research team led by Dr. George A. Ricaurte at Johns Hopkins University implicated MDMA as a cause of Parkinson's-like brain abnormalities in monkeys, suggesting that a single use of MDMA caused permanent and serious brain damage. These claims were hotly disputed by physicians, therapists, and other experts in the field, including a team of scientists at New York University. Criticisms of the study included its use of injection rather than oral administration; that this type and scale of damage (>20% mortality) would translate to hundreds of thousands or millions of deaths which had not materialized in the real world amidst extremely broad global MDMA usage; and, perhaps most important, that other research teams could not duplicate the study's findings.
On September 6, 2003, Dr. George A. Ricaurte and his team announced that they were retracting all results of their commonly cited and controversial study. The researchers said that the labels on the drugs had been somehow switched, and they had inadvertently injected their experimental monkeys and baboons with extremely high doses of methamphetamine instead of MDMA. The chemical supplier, Research Triangle Institute, has publicly claimed that the proper drug was supplied, and Ricaurte has yet to pursue them for their alleged error.
Ricaurte had also come under fire for supplying PET scans to the U.S. Office of National Drug Control Policy that were used in anti-drug literature (Plain Brain/Brain After Ecstasy) that seemed to suggest MDMA created holes in human brains, an implication that critics called misleading. Ricaurte later asked the Agency to change the literature, citing the "poor quality" of the images. These images are still circulating in educational systems across the U.S., however, and the myth that ecstasy users develop "holes in their brains" remains quite popular.
[sửa] Vấn đề pháp lý
Use, supply and trafficking of ecstasy are currently illegal in most countries. In the United States, MDMA was legal and unregulated until May 31st 1985, at which time it was added to DEA Schedule I, for drugs deemed to have no medical uses and a high potential for abuse. During DEA hearings to criminalize MDMA, most experts recommended DEA Schedule III prescription status for the drug, due to its beneficial usage in psychotherapy. The judge overseeing the hearings, Francis Young, also made this recommendation. Nonetheless, the DEA classified it as Schedule I[4].
That same year, the World Health Organization's Expert Committee on Drug Dependence recommended that MDMA be placed in Schedule I of the Convention on Psychotropic Substances. Unlike the Controlled Substances Act, the Convention has a provision (in Article 7(a)) that allows use of Schedule I drugs for "scientific and very limited medical purposes". The Committee's report stated[2]:
- It should be noted that the Expert Committee held extensive discussions concerning therapeutic usefulness of 3,4 Methylenedioxymethamphetamine. While the Expert Committee found the reports intriguing, it felt that the studies lacked the appropriate methodological design necessary to ascertain the reliability of the observations. There was, however, sufficient interest expressed to recommend that investigations be encouraged to follow up these preliminary findings. To that end, the Expert Committee urged countries to use the provisions of article 7 of the Convention on Psychotropic Substances to facilitate research on this interesting substance.
In the United Kingdom, MDMA is Schedule I/Class A, making it illegal to sell, buy, or possess without a license. Penalties include a maximum of seven years and/or unlimited fine for possession; life and/or unlimited fine for production or trafficking. A mandatory seven year sentence is now the penalty for a third conviction for trafficking.
[sửa] Sử dụng trong y học
In 2001, the FDA approved MDMA for research with patients suffering from post-traumatic stress disorder. In March of 2004, the DEA issued its first Schedule I possession licenses for those conducting research under the FDA approval; research is being conducted through the Multidisciplinary Association for Psychedelic Studies (MAPS) on veterans from the U.S. invasion of Afghanistan, rape victims, and cancer patients. For further information on this, see MAPS's MDMA Research Information and the recent article from MSNBC/Newsweek.
[sửa] Tính an toàn
The illegality of this drug in many countries makes exact study of its effects difficult. Some of the effects ascribed to ecstasy, which may or may not be conclusive, are the following:
- Because of its illegality, the dose and purity of a pill advertised as ecstasy may be stronger than is desired or may be unsafe.
- Ecstasy affects the regulation of the body's internal systems. Continuous dancing without sufficient breaks or drinks can lead to dangerous overheating and dehydration. Drinking too much water without consuming a corresponding amount of salt can lead to hyponatremia or Water intoxication.
- The use of ecstasy can exacerbate depression and may produce temporary depression as an after-effect for some users. Some individuals also might experience wild or unexpected mood swings the first couple of days following the use of MDMA.
- The use of ecstasy can be very dangerous when combined with other drugs (particularly monoamine oxidase inhibitors (MAOIs) and antiretroviral drugs, in particular Ritonavir).
- In many cases, pills marketed as ecstasy do not contain MDMA, but instead are substituted with various substances like ketamine, methamphetamine and caffeine. Some users purchase testing kits to verify that pills are actually MDMA. Organizations such as DanceSafe provide testing kits [3].
- Long-term after-effects are greatly exacerbated by high doses and frequent use.
- A small percentage of users may be highly sensitive to MDMA; this may make first-time use especially hazardous. This includes but is not limited to people with congenital heart defects, and a small percentage of people who lack the proper enzymes to break down the drug. The enzyme responsible for MDMA's breakdown is CYP2D6,which is deficient or totally absent in 5-10% of whites and people of African descent and 1-2% of Asians.[4]
[sửa] Xem thêm
[sửa] Truyền thông đại chúng
- Jennings, Peter. "Primetime Special: Peter Jennings - Ecstasy Rising." ABC News, April 1, 2004.
- Conant, Eve. "Ecstasy: A Possible New Role for a Banned Club Drug." Newsweek, May 2, 2005.
- Generation on X: An undercover look at the growing trend of teens using Ecstasy FOX News, April 26, 2005.
- Weiss, Rick. "Use Studied to Ease Fear in Terminally Ill." The Washington Post, December 27, 2004.
- Philipkoski, Kristen. "Long Trip for Psychedelic Drugs." Wired, September 27, 2004.
- Philipkoski, Kristen. "DEA Approves Ecstasy Tests." Wired, March 2, 2004.
- Darman, Jonathan. "Out of the Club, Onto the Couch Newsweek.com, December 5, 2003. - An interview with NYU's Dr. Julie Holland
- Weiss, Rick. "Results Retracted on Ecstasy Study." The Washington Post, September 6, 2003.
- Recer, Paul "Ecstasy-Parkinson's Connections?."CBS News, September 26, 2002.
- Man found to have taken 40,000 tabs in 9 years - London.; The Guardian, April 4, 2006.
- Wittlin, Maggie. "Hitting a High E: Italian scientists find loud music intensifies and extends the brain’s response to MDMA," Seed Magazine (02/15/2006)
[sửa] Những nghiên cứu khoa học
- Ecstasy có hại cho thai nhi
- Thuốc lắc có thể trở thành một dược phẩm?
- The Multidisciplinary Association for Psychedelic Studies (MAPS): MDMA project MAPS is at the forefront of human MDMA research, having obtained FDA permits for two studies administering MDMA to human volunteers in order to explore the drug's potential psychiatric benefits (one study is already underway.)
- The DEA.org's extensive critique/review of the evidence against MDMA ('ecstasy') causing brain damage at common recreational doses.
- This is your brain on Ecstasy - A slideshow that illustrates the neuropharmacokinetics of Ecstasy (how the drug affects the brain.) Some of the information on this page is at present (July 2005) outdated.
- PiHKAL entry
- The MAPS research library, containing downloadable copies of most of the MDMA and LSD research ever done.
[sửa] Chung
- Multidisciplinary Association for Psychedelic Studies - A non-profit organization currently conducting FDA-approved studies with MDMA.
- EcstasyData.org A database of photos and lab-test results of over 1500 pills of "Ecstasy".
- Pillreports A similar database to EcstasyData, but with user-contributed photos of pills and subjective "pill reports" and ratings. Over 1600 listings (as of Jan. 2006).
- DanceSafe - a risk reduction site with lots of information on Ecstasy. Includes a large database of photographs of different pill types, along with laboratory analysis of what was actually found in the pill.
- Erowid's Ecstasy page - lots of information
- UK National Drugs Line factsheet on Ecstasy
- American Council for Drug Education factsheet on Ecstasy
- Congressional Research Service (CRS) Reports regarding Ecstasy
- http://www.ecstasy.org
- Utopian Pharmacology. Detailed essay discussing the history and uses of MDMA
- TheDEA.org An ecstasy user's guide with detailed discussions of risks and scientific research.
- MDMA, Personality and Human Nature: The Power to Transform People. Essay by Bruce Eisner, author of Ecstasy: The MDMA Story
- My Daughter's Good Death - Ecstasy as a Tool for End of Life (adult content)
- ▲ The Ecstasy Testing Program
- ▲ Baumann MH, Wang X, Rothman RB. (2006). “3,4-Methylenedioxymethamphetamine (MDMA) neurotoxicity in rats: a reappraisal of past and present findings.”. Psychopharmacology.
- ▲ Saunders, Nicholas (1995). Interviews with two foremost researchers into neurotoxicity who hold opposing views.
- ▲ MAPS. Documents from the DEA Scheduling Hearing of MDMA, 1984-1988.
- Baggott, Matthew, and John Mendelson. “MDMA Neurotoxicity”. Ecstasy: The Complete Guide. Ed. Julie Holland. Spring 2001 from www.erowid.com.
- de la Torre, Rafael et al. (2000), Non-linear pharmacokinetics of MDMA (`ecstasy') in humans. Br J Clin Pharmacol, 2000; 49(2):104-9
- de la Torre, Rafael & Farré, Magí (2004). Neurotoxicity of MDMA (ecstasy): the limitations of scaling from animals to humans. Trends in Pharmacological Sciences 25, 505-508.
- Erowid, Earth. “Do Antioxidants Protect Against MDMA Hangover, Tolerance, and Neurotoxicity?” Erowid Extracts. Dec 2001; 2:6-11.
- Jennings, Peter. Ecstasy Rising, ABC television documentary. 2004-01-04.
- Jones, Douglas C. et al. (2004). Thioether Metabolites of 3,4-Methylenedioxyamphetamine and 3,4-Methylenedioxymethamphetamine Inhibit Human Serotonin Transporter (hSERT) Function and Simultaneously Stimulate Dopamine Uptake into hSERT-Expressing SK-N-MC Cells. J Pharmacol Exp Ther 311, 298-306.
- Kalant H. (2001) The pharmacology and toxicology of "ecstasy" (MDMA) and related drugs. CMAJ. Oct 2;165(7):917-28. Review. PMID 11599334 Full Text
- Miller, R.T. et al. (1997). 2,5-Bis-(glutathione-S-yl)-alpha-methyldopamine, a putative metabolite of (+/-)-3,4-methylenedioxyamphetamine, decreases brain serotonin concentrations. Eur J Pharmaco. 323(2-3), 173-80. Abstract retrieved Apr 17, 2005, from PubMed.
- Monks, T.J. et al. (2004). The role of metabolism in 3,4-(+)-methylenedioxyamphetamine and 3,4-(+)-methylenedioxymethamphetamine (ecstasy) toxicity. Ther Drug Monit 26(2), 132-136.
- Morgan, Michael John (2000). Ecstasy (MDMA): a review of its possible persistent psychological effects. Psychopharmacology 152, 230-248.
- Shankaran, Mahalakshmi, Bryan K. Yamamoto, and Gary A. Gudelsky. “Ascorbic Acid Prevents 3,4,-Methylenedioxymethamphetamine (MDMA)- Induced Hydroxyl Radical Formation and the Behavioral and Neurochemical Consequences of the Depletion of Brain 5-HT”. Synapse. 2001; 40:55-64.
- Strote, Jared et al. (2002). Increasing MDMA use among college students: results of a national survey. Journal of Adolescent Health 30, 64-72.
- Sumnall, Harry R. & Cole, Jon C. (2005). Self-reported depressive symptomatology in community samples of polysubstance misusers who report Ecstasy use: a meta-analysis. Journal of Psychopharmacology 19(1), 84-92.
Yeh, S. Y. “Effects of Salicylate on 3,4-Methylenedioxymethamphetamine (MDMA)-Induced Neurotoxicity in Rats”. Pharmacology Biochemistry and Behavior. 1997; Vol. 58, No. 3: 701-708.Tiêu bản:Entactogens Tiêu bản:Amphetamines Tiêu bản:Hallucinogenic phenethylamines
