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The pharmacology and clinical pharmacology of 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy").
Pharmacol Rev. 2003 Sep; 55(3):463-508.PR

Abstract

The amphetamine derivative (+/-)-3,4-methylenedioxymethamphetamine (MDMA, ecstasy) is a popular recreational drug among young people, particularly those involved in the dance culture. MDMA produces an acute, rapid enhancement in the release of both serotonin (5-HT) and dopamine from nerve endings in the brains of experimental animals. It produces increased locomotor activity and the serotonin behavioral syndrome in rats. Crucially, it produces dose-dependent hyperthermia that is potentially fatal in rodents, primates, and humans. Some recovery of 5-HT stores can be seen within 24 h of MDMA administration. However, cerebral 5-HT concentrations then decline due to specific neurotoxic damage to 5-HT nerve endings in the forebrain. This neurodegeneration, which has been demonstrated both biochemically and histologically, lasts for months in rats and years in primates. In general, other neurotransmitters appear unaffected. In contrast, MDMA produces a selective long-term loss of dopamine nerve endings in mice. Studies on the mechanisms involved in the neurotoxicity in both rats and mice implicate the formation of tissue-damaging free radicals. Increased free radical formation may result from the further breakdown of MDMA metabolic products. Evidence for the occurrence of MDMA-induced neurotoxic damage in human users remains equivocal, although some biochemical and functional data suggest that damage may occur in the brains of heavy users. There is also some evidence for long-term physiological and psychological changes occurring in human recreational users. However, such evidence is complicated by the lack of knowledge of doses ingested and the fact that many subjects studied are or have been poly-drug users.

Authors+Show Affiliations

AstraZeneca R&D Charnwood, Loughborough, LE11 5RH, UK. richard.green@astrazeneca.comNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

12869661

Citation

Green, A Richard, et al. "The Pharmacology and Clinical Pharmacology of 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy")." Pharmacological Reviews, vol. 55, no. 3, 2003, pp. 463-508.
Green AR, Mechan AO, Elliott JM, et al. The pharmacology and clinical pharmacology of 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy"). Pharmacol Rev. 2003;55(3):463-508.
Green, A. R., Mechan, A. O., Elliott, J. M., O'Shea, E., & Colado, M. I. (2003). The pharmacology and clinical pharmacology of 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy"). Pharmacological Reviews, 55(3), 463-508.
Green AR, et al. The Pharmacology and Clinical Pharmacology of 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy"). Pharmacol Rev. 2003;55(3):463-508. PubMed PMID: 12869661.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The pharmacology and clinical pharmacology of 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy"). AU - Green,A Richard, AU - Mechan,Annis O, AU - Elliott,J Martin, AU - O'Shea,Esther, AU - Colado,M Isabel, Y1 - 2003/07/17/ PY - 2003/7/19/pubmed PY - 2003/12/19/medline PY - 2003/7/19/entrez SP - 463 EP - 508 JF - Pharmacological reviews JO - Pharmacol Rev VL - 55 IS - 3 N2 - The amphetamine derivative (+/-)-3,4-methylenedioxymethamphetamine (MDMA, ecstasy) is a popular recreational drug among young people, particularly those involved in the dance culture. MDMA produces an acute, rapid enhancement in the release of both serotonin (5-HT) and dopamine from nerve endings in the brains of experimental animals. It produces increased locomotor activity and the serotonin behavioral syndrome in rats. Crucially, it produces dose-dependent hyperthermia that is potentially fatal in rodents, primates, and humans. Some recovery of 5-HT stores can be seen within 24 h of MDMA administration. However, cerebral 5-HT concentrations then decline due to specific neurotoxic damage to 5-HT nerve endings in the forebrain. This neurodegeneration, which has been demonstrated both biochemically and histologically, lasts for months in rats and years in primates. In general, other neurotransmitters appear unaffected. In contrast, MDMA produces a selective long-term loss of dopamine nerve endings in mice. Studies on the mechanisms involved in the neurotoxicity in both rats and mice implicate the formation of tissue-damaging free radicals. Increased free radical formation may result from the further breakdown of MDMA metabolic products. Evidence for the occurrence of MDMA-induced neurotoxic damage in human users remains equivocal, although some biochemical and functional data suggest that damage may occur in the brains of heavy users. There is also some evidence for long-term physiological and psychological changes occurring in human recreational users. However, such evidence is complicated by the lack of knowledge of doses ingested and the fact that many subjects studied are or have been poly-drug users. SN - 0031-6997 UR - https://www.unboundmedicine.com/medline/citation/12869661/The_pharmacology_and_clinical_pharmacology_of_34_methylenedioxymethamphetamine__MDMA_"ecstasy"__ L2 - http://pharmrev.aspetjournals.org/cgi/pmidlookup?view=long&pmid=12869661 DB - PRIME DP - Unbound Medicine ER -