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Further human evidence for striatal dopamine release induced by administration of ∆9-tetrahydrocannabinol (THC): selectivity to limbic striatum

Research output: Contribution to journalArticle

Matthijs Bossong, Mitul Mehta, Bart van Berckel, Oliver Howes, Rene S. Kahn, Paul Stokes

Original languageEnglish
Pages (from-to)2723-2729
Number of pages7
JournalPsychopharmacology
Volume232
Issue number15
DOIs
Publication statusPublished - Aug 2015

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Abstract

Rationale: Elevated dopamine function is thought to play a key role in both the rewarding effects of addictive drugs and the pathophysiology of schizophrenia. Accumulating epidemiological evidence indicates that cannabis use is a risk factor for the development of schizophrenia. However, human neurochemical imaging studies that examined the impact of ∆9-tetrahydrocannabinol (THC), the main psychoactive component in cannabis, on striatal dopamine release have provided inconsistent results.
Objectives: To assess the effect of a THC challenge on human striatal dopamine release in a large sample of healthy participants.
Methods: We combined human neurochemical imaging data from two previous studies that used [11C]raclopride positron emission tomography (PET) (n=7 and n=13, respectively) to examine the effect of THC on striatal dopamine neurotransmission in humans. PET images were re-analysed to overcome differences in PET data analysis.
Results: THC administration induced a significant reduction in [11C]raclopride binding in the limbic striatum (-3.65%, from 2.390.26 to 2.300.23, p=0.023). This is consistent with increased dopamine levels in this region. No significant differences between THC and placebo were found in other striatal subdivisions.
Conclusions: In the largest data set of healthy participants so far, we provide evidence for a modest increase in human striatal dopamine transmission after administration of THC compared to other drugs of abuse. This finding suggests limited involvement of the endocannabinoid system in regulating human striatal dopamine release, and thereby challenges the hypothesis that an increase in striatal dopamine levels after cannabis use is the primary biological mechanism underlying the associated higher risk of schizophrenia.

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