superqt4u2nv said:
I would be interested in reading it for sure thanks!
I was looking around- most of it was pretty dry... I can't access full articles to post them up (as I am not at a university)... but the articles below looked like decent reviews to look up if you are able..
It has been implicated in damaging serotonin, dopamine, acetocholine neural pathways (neural damage) and even implicated in damaging glucose uptake (sugars are the only things your brain can use as fuel)
........the first time I did it I was out and about partying with a buddy of mine (who eventually became a surgeon)..... the funny thing is right after we took it he says to me "what is crazy is we just burned up like 40% of our serotonin receptors" (which is what I had learned previously in school) ... we shared an uncomfortable laugh after that....
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Pharmacol Rev. 2003 Sep;55(3):463-508. Epub 2003 Jul 17.
The pharmacology and clinical pharmacology of 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy").
Green AR, Mechan AO, Elliott JM, O'Shea E, Colado MI.
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.
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Hum Psychopharmacol. 2001 Dec;16(8):557-577. Related Articles, Links
Human psychopharmacology of Ecstasy (MDMA): a review of 15 years of empirical research.
Parrott AC.
Department of Psychology, University of East London, UK.
MDMA (3,4-methylenedioxymethamphetamine) or 'Ecstasy' was scheduled as an illegal drug in 1986, but since then its recreational use has increased dramatically. This review covers 15 years of research into patterns of use, its acute psychological and physiological effects, and the long-term consequences of repeated use. MDMA is an indirect monoaminergic agonist, stimulating the release and inhibiting the reuptake of serotonin (5-HT) and, to a lesser extent, other neurotransmitters. Single doses of MDMA have been administered to human volunteers in double-blind placebo-controlled trials, although most findings are based upon recreational MDMA users. The 'massive' boost in neurotransmitter activity can generate intense feelings of elation and pleasure, also hyperactivity and hyperthermia. This psychophysiological arousal may be exacerbated by high ambient temperatures, overcrowding, prolonged dancing and other stimulant drugs. Occasionally the 'serotonin syndrome' reactions may prove fatal. In the days after Ecstasy use, around 80% of users report rebound depression and lethargy, due probably to monoaminergic depletion. Dosage escalation and chronic pharmacodynamic tolerance typically occur in regular users. Repeated doses of MDMA cause serotonergic neurotoxicity in laboratory animals, and there is extensive evidence for long-term neuropsychopharmacological damage in humans. Abstinent regular Ecstasy users often display reduced levels of 5-HT, 5-HIAA, tryptophan hydroxylase and serotonin transporter density; functional deficits in learning/memory, higher cognitive processing, sleep, appetite and psychiatric well-being, and, most paradoxically, 'loss of sexual interest/pleasure'. These psychobiological deficits are greatest in heavy Ecstasy users and may reflect serotonergic axonal loss in the higher brain regions, especially the frontal lobes, temporal lobes and hippocampus. These problems seem to remain long after the recreational use of Ecstasy has ceased, suggesting that the neuropharmacological damage may be permament. Copyright 2001 John Wiley & Sons, Ltd.
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