The purpose of this study is to determinate the effect of a pre-treatment with centrally acting alpha2-receptor agonist clonidine on the pharmacodynamics and pharmacokinetics of 3,4-methylenedioxymethamphetamine (MDMA, “Ecstasy”). The investigators hypothesize that clonidine will attenuate the subjective and cardiovascular response to MDMA.
Topic Healthy Subjects
Country Switzerland
Visit trial
Status
Completed
Results Published
Start date
07 January 2010
End date
12 January 2010
Chance of happening
100%
Phase
Phase I
Design
Blinded
Type
Interventional
Generation
First
Participants
16
Sex
All
Age
18- 45
Therapy
No
Trial Details
3,4-methylenedioxymethamphetamine (MDMA, "ecstasy") is widely used by young people for its euphoric effects. MDMA releases serotonin (5-HT), norepinephrine (NE), and dopamine. It is unknown which of these monoamines mainly contributes to the subjective and physiological effects of MDMA in humans. Clonidine is a centrally acting alpha2-receptor agonist and sympatholytic which attenuates the release of NE from presynaptic nerve terminals and also lowers NE plasma concentration. To determine the role of NE in the response to MDMA in humans we test the effects of a clonidine pretreatment on the pharmacodynamics and pharmacokinetics of MDMA. We use a randomized double-blind placebo-controlled cross-over design with four experimental sessions. Clonidine (150 μg) or placebo will be administered 1 h before the administration of MDMA (125 mg) or placebo to 16 healthy volunteers. Subjective and cardiovascular responses will be repeatedly assessed throughout the experiments and plasma samples are collected for pharmacokinetics. We hypothesize that clonidine will significantly attenuate predominantly the cardiovascular response to MDMA.NCT Number NCT01136278
Sponsors & Collaborators
University of BaselThe University of Basel Department of Biomedicine hosts the Liechti Lab research group, headed by Matthias Liechti.
Papers
Effects of MDMA alone and after pretreatment with reboxetine, duloxetine, clonidine, carvedilol, and doxazosin on pupillary light reflexThis study analysed data from five separate clinical trials (n=80) that explored the effects of MDMA on pupillary light reflex and the effects following pretreatment with reboxetine, duloxetine, clonidine, carvedilol, and doxazosin, respectively. MDMA produced mydriasis, prolonged the latency, reduced the response to light and shortened the recovery time and this impairment returned to normal 6 hours post-treatment. Only reboxetine and duloxetine interacted with the effects of MDMA on pupillary function.