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Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. In animals, pretreatment with 5-HT 2 antagonists has been shown to attenuate neurochemical and behavioral effects of MDMA. Subjective effects were rated by psychometric rating scales. Physiological effects measured were blood pressure, heart rate, and body temperature. Adverse effects were assessed during the sessions, and after one and three days. Ketanserin attenuated MDMA-induced perceptual changes, emotional excitation, and acute adverse responses but had little effect on MDMA-induced positive mood, well-being, extroversion, and short-term sequelae. In humans, MDMA produces enhanced mood with increased well-being and extroversion, moderate derealization and slight perceptual changes Peroutka et al. The physiological response to MDMA includes elevated blood pressure and heart rate, a slight increase in psychomotor drive, and side effects such as jaw clenching, lack of appetite, and difficulty concentrating Mas et al. The roles of different neurotransmitters and receptors in mediating these effects of MDMA in humans are unclear. We have recently used the 5-HT uptake inhibitor citalopram and the dopamine D 2 antagonist haloperidol as pretreatments to MDMA in healthy subjects. Citalopram largely reduced subjective Liechti et al. These results support the hypothesis that the effects of MDMA in humans are largely dependent on 5-HT transporter-mediated enhancement of serotonergic neurotransmission. Animal studies indicate that 5-HT 2 receptors might be involved, because 5-HT 2 antagonists reduced several effects of MDMA, such as MDMA-induced serotonergic neurotoxicity, acute hyperthermia and disruption of sensorimotor gating Padich et al. Based on this evidence, we expected that also in humans some effects of MDMA would be reduced by pretreatment with a 5-HT 2 antagonist. We expected that ketanserin would attenuate some of the MDMA effects, particularly its moderate hallucinogen-like properties. All subjects were screened by a semi-structured psychiatric interview and were healthy according to history, physical examination, electrocardiogram, and blood analysis. Exclusion criteria were as follows: personal or family history of major psychiatric disorder in first-degree relatives, somatic illness and regular alcohol or substance abuse. Fourteen volunteers 13 men, 1 woman were finally included in the study. Seven had smoked cannabis a few times and four had once tried a hallucinogen. All volunteers gave their written consent after being informed by written and oral descriptions of the aim of the study, the procedures involved, and the effects and possible risks of MDMA administration. Subjects were paid for their participation. This study utilized a double-blind, placebo-controlled counterbalanced within-subjects design with four experimental conditions: placebo—placebo, ketanserin—placebo, placebo—MDMA or ketanserin—MDMA. The four sessions were separated by at least 10 days to reduce carry-over effects. Test sessions were conducted in a calm and comfortable laboratory environment. Participants were told not to eat 2 h prior to each session. At the beginning of each session volunteers took ketanserin 50 mg or placebo capsules. After 75 min MDMA 1. Psychometric ratings were performed before, shortly after drug onset and during the peak effect i. Blood pressure, heart rate and peripheral body temperature were measured 75 min before and 0, 60, 90, , and min after MDMA or placebo intake. This scale consists of 66 items yielding a global score measuring physical and general discomfort. Acute drug effects were assessed during the session, short-term sequelae the next day 24 h and again three days after the test session 72 h. In addition, sensorimotor gating of the acoustic startle reflex was measured data not shown. At the end of the study all subjects attended a debriefing interview including a retrospective comparative evaluation of their subjective experience of all four study sessions. The STAI yields a score for state and trait anxiety levels. The trait scale was administered prior to entering the study. The state scale was used during each session. Ketanserin was kindly provided by Janssen-Cilag AG Switzerland and was prepared as gelatine capsules of 50 mg. Subjects received MDMA at a single dose of 1. This dose has robust psychological and physiological effects and was carefully evaluated to minimize possible risks Vollenweider et al. Data were analyzed using Statistica 5. Tukey's post hoc tests were performed based on significant main effects or interactions. F- and p -values for significant main effects and interactions are presented in Table 1. Subjective effects of MDMA 1. MDMA produced robust effects on all measures, except for state-anxiety which was not significantly changed. MDMA significantly increased scores in all five scales. MDMA also induced a significant, although slight, increase in auditory alterations. Auditory perception was qualitatively changed e. Vigilance was reduced by MDMA and interestingly, this effect was less pronounced after ketanserin. Mean and S. Figure 2 shows peak scores of all scales of the AM mood rating. Similarly, MDMA-induced extroversion was not significantly changed. As shown in Table 1 and Figure 3 , MDMA significantly increased blood pressure, heart rate and peripheral body temperature. As seen in Figure 3 , levels of peripheral body temperature were lowered to levels of placebo when MDMA and ketanserin were given together. Ketanserin alone also lowered values compared to placebo. Acute side effects and short-term sequelae are listed in Table 2. Ketanserin significantly reduced the total of acute adverse responses to MDMA, but not short-term sequelae, as assessed after 24 and 72 h. Ketanserin alone produced very little adverse effects. A debriefing interview after completion of the study revealed that only 5 of 14 subjects could distinguish ketanserin from placebo. Nine of 14 subjects retrospectively reported that their MDMA experience was clearly less intense after ketanserin pretreatment. Five participants subjectively felt little difference between MDMA and MDMA plus ketanserin and were therefore not sure when they had received which treatment. This finding is consistent with several lines of evidence that indole hallucinogens exert their effects via agonist action at 5-HT 2A receptors Glennon ; Titeler et al. For example, it has been shown that the binding affinity for a drug for the 5-HT 2A receptor site predicts its potency for evoking hallucinations in humans Glennon et al. We have recently shown that the selective serotonin uptake inhibitor citalopram markedly reduced both psychological and physiological responses to MDMA in healthy volunteers Liechti et al. These results indicate that MDMA effects are largely dependent on transporter-mediated release of serotonin. This failure to block all effects of MDMA could be due to an insufficient dose of ketanserin. We cannot address this possibility because we used only one dose of ketanserin which, however, has proved to be effective in psilocybin subjects Vollenweider et al. The fact that ketanserin showed a relative selectivity in reducing alterations in the OAVAV scale compared to citalopram supports the involvement of 5-HT 2 receptors in mediating perceptual changes induced by released serotonin. On the other hand, only citalopram Liechti et al. Emotional excitation in the present study was reduced by ketanserin pretreatment. In contrast, pretreatment with the D 2 antagonist haloperidol failed to reduce MDMA-induced emotional excitation in an identical study design Liechti and Vollenweider b. Pretreatment with citalopram was also ineffective in this regard Liechti et al. These findings suggest that MDMA-induced emotional excitation is not primarily dependent on release of endogenous serotonin or D 2 receptor stimulation. There are several possible explanations for this unexpected result. Dopamine is generally thought to be involved in the euphoriant and arousing effects of stimulants such as d-amphetamine and cocaine Vollenweider et al. Thus, the stimulant-like properties of MDMA may be attributed partially to 5-HT 2 -mediated increase of dopamine activity. In particular, such indirect dopamine activation might have contributed to emotional excitation induced by MDMA in the present study. A role for D 1 -like receptors has also been suggested for the mediation of the acute mood altering effects of cocaine in humans Romach et al. Several subjects in the present study reported that dysphoric effects of MDMA coexisted or alternated with its pleasurable effects. Indeed, MDMA also increased scores for vigilance reduction, dazed state, inactivation, apprehension-anxiety, and produced several adverse effects. H 1 antagonists are well known for their adverse effects including sedation and dizziness. Thus, H 1 receptors are likely to be involved in the mediation of such unpleasant responses to MDMA and ketanserin. Ketanserin lowered diastolic blood pressure and body temperature when given as a pretreatment to MDMA but also when given alone compared to placebo. Although there was no statistical interaction of MDMA and ketanserin in the present study, the complete reduction of MDMA-induced increases in body temperature is consistent with animal studies demonstrating that 5-HT 2 antagonists such as MDL 11, or ketanserin block the hyperthermic effect of MDMA in rats Schmidt et al. In particular, our results indicate that the mild hallucinogen-like perceptual effects of MDMA in humans may be mediated via 5-HT 2 receptors. Eur J Pharmacol : — Drugs 40 : — Dittrich A. Pharmacopsychiat 31 : 80— Article Google Scholar. Summary of the results. Germ J Psych 9 : — Google Scholar. Geyer MA. Neuropsychopharmacology 10 : S. Glennon RA. Neuropsychopharmacology 3 : — Life Sciences 35 : — Janke W, Debus G. J Nuc Med 36 : — CAS Google Scholar. Life Sciences 28 : — Neuropsychopharmacology 21 : — Neuropsychopharmacology 22 : — J Psychopharmacol in press. European Neuropsychopharmacology 10 : — J Pharmacol Exp Ther : — Nash JF. Life Sciences 47 : — Psychopharmacology 84 : — Psychopharmacology : — Neuropsychopharmacology 1 : — Arch Gen Psychiatry 56 : — Rudnick G, Wall SC. Proc Natl Acad Sci 89 : — Am J Psychiatry : — Brain Res : 85— Eur J Pharmacol : 65— Ann NY Acad Sci : — Biochem Pharmacol 36 : — J Neurochem 62 : — Psychiatry Res 27 : — Psychopharmacology ;94 : — Nature : — Neuropsychopharmacology 19 : — NeuroReport 9 : — Psychiatry Research: Neuroimaging 83 : — Zerssen DV. Download references. The authors especially thank Mark A. Geyer, San Diego, for critical comments on the manuscript. You can also search for this author in PubMed Google Scholar. Reprints and permissions. Liechti, M. Neuropsychopharmacol 23 , — Download citation. Received : 29 November Revised : 23 February Accepted : 29 March Issue Date : 01 October Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content Thank you for visiting nature. Download PDF. Study Design This study utilized a double-blind, placebo-controlled counterbalanced within-subjects design with four experimental conditions: placebo—placebo, ketanserin—placebo, placebo—MDMA or ketanserin—MDMA. Data Analysis Data were analyzed using Statistica 5. Figure 1. Full size image. Figure 2. Figure 3. Table 2 Full size table. View author publications. Rights and permissions Reprints and permissions. About this article Cite this article Liechti, M. Copy to clipboard. Kuypers R. Ramaekers Psychopharmacology Search Search articles by subject, keyword or author. 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Non-linear pharmacokinetics of MDMA (‘ecstasy’) in humans

Bern buy Ecstasy

In Switzerland clubbers can get recreational drugs tested to help them make a more 'informed choice' before using them. There is no such system in the UK although 'front of house' testing has been trialled at two festivals in We went to the Swiss city of Bern to see a pop-up centre where clubbers get their drugs screened weekly. And we followed a tablet from drop-off to testing and back to the user for results. First we meet year-old clubber 'John' as he drops off a pill for testing. He says he bought it from friends and he believes it is ecstasy. John is greeted by drug councillor Nik Hostettler who goes through John's current use and asks two main questions: when he plans to take the pill and whether it will be consumed along with other substances. Then John hands the pill to a scientist from a local government-approved laboratory. A scientist takes a quarter of the pill and gives the rest back to John. The sample is then crushed with a pestle and mortar and put into a glass tube. The tester then asks for more information about the pill including its price and its source. It all happens at an anonymous-looking office on the outskirts of the city centre. The next day at a government laboratory the crushed-up pill is weighed and a small amount of it is dissolved in a solvent. This is then analysed in a liquid chromatography machine. Another measurement is taken to calculate the strength of whatever substance is being tested. Fabienne Holzer, who is carrying out the testing, confirms it is a very strong ecstasy pill. Holzer's boss is watching on and is quick to emphasise the findings. The results are then sent to the councillor so he can feed them back to John who dropped the pill off. John then calls up to get the result for his pill and he gets advice on how to minimise the risk if he decides to take it. It's a very high dose but it doesn't have anything different in it. Drug experts warn that ecstasy is the strongest it has been in years and there's been a warning that it is causing the biggest risk to users' mental health in decades. How the pill was tested. The pill is in the shape of an owl. This conversation takes around 20 minutes. He then measures and photographs it. The results come out as a reading on a graph. They are compared with known drug patterns.

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