Functional Brain Imaging in Recreational Users of Ecstasy

This observational study (n=18) of recreational MDMA users (unknown quantity/regularity) shows that those who use MDMA have lower levels of dopamine release in the test (motorbike riding computer game). The participants didn’t differ in reaction time (performance).

The results from the study, which focussed on game addiction, state:

“The brain imaging study showed that healthy control subjects had reduced dopamine D2 receptor occupancy of 10.5% in the caudate after playing a motorbike riding computer game compared with baseline levels of binding consistent with increased release and binding to its receptors. Ex-chronic “ecstasy” users showed no change in levels of dopamine D2 receptor occupancy after playing this game. Conclusion: This evidence supports the notion that psycho-stimulant users have decreased sensitivity to natural reward. Significance: Computer game addicts or gamblers may show reduced dopamine response to stimuli associated with their addiction presumably due to sensitization.“

Trial Details

Recreational use of "ecstasy" (MDMA; 3, 4-Methylenedioxymethamphetamine) is associated with long-lasting effects on metabolism in the human brain. In particular, there is evidence of long-term damage to the brains' neurotransmitter serotonin (5-HT). It is also known that chronic use of Methamphetamine (which is similar in its chemical structure to "ecstasy") is linked to impaired cognitive and motor skills despite recovery of dopamine transporters (DAT). We have investigated whether chronic use of "ecstasy" is causing any impairment in motor skills and function of the dopaminergic system in recreational users of "ecstasy". In our preliminary study, we have scanned control subjects and "ecstasy" users, at baseline and after performing on a motorbike riding computer game while imaging dopamine in vivo with [123I] IBZM (a D2 receptor radiotracer) in Single Photon Emission Computed Tomography (SPECT). We showed: Lower measures of D2 at baseline in ecstasy users compared with control subjects, that means lower level of dopaminergic activity in "ecstasy" users. Significant displacement of [123I] IBZM by endogenous dopamine released during the game in healthy subjects unlike "ecstasy" users, that means that recreational users of "ecstasy" release much less natural dopamine. No difference between the groups in performance (reaction time) on riding the game after a year of recovery. Our results show preliminary evidence for dopaminergic deficiency in "ecstasy" users, a finding that has not been shown before. However, similar to other drugs of abuse, it is not known whether dopaminergic deficiency is the cause or consequence of the use of "ecstasy". We now propose to proceed to scan more recreational users of "ecstasy" in order to assess whether chronic use of "ecstasy" is associated with deficient dopaminergic neurotransmission in the brain.

NCT Number NCT00254306

Data attribution

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