Dopaminergic Function in Cannabis Users and Its Relationship to Cannabis-Induced Psychotic Symptoms

Michael A. P. Bloomfield, Celia J. A. Morgan, Alice Egerton, Shitij Kapur, H. Valerie Curran, Oliver D. Howes*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

158 Citations (Scopus)

Abstract

Background: Cannabis is the most widely used illicit drug globally, and users are at increased risk of mental illnesses including psychotic disorders such as schizophrenia. Substance dependence and schizophrenia are both associated with dopaminergic dysfunction. It has been proposed, although never directly tested, that the link between cannabis use and schizophrenia is mediated by altered dopaminergic function.

Methods: We compared dopamine synthesis capacity in 19 regular cannabis users who experienced psychotic-like symptoms when they consumed cannabis with 19 nonuser sex-and age-matched control subjects. Dopamine synthesis capacity (indexed as the influx rate constant K-i(cer)) was measured with positron emission tomography and 3,4-dihydroxy-6-[F-18]-fluoro-l-phenylalanine ([F-18]-DOPA).

Results: Cannabis users had reduced dopamine synthesis capacity in the striatum (effect size:.85; t(36) = 2.54, p = .016) and its associative (effect size:.85; t(36) = 2.54, p = .015) and limbic subdivisions (effect size:.74; t(36) = 2.23, p = .032) compared with control subjects. The group difference in dopamine synthesis capacity in cannabis users compared with control subjects was driven by those users meeting cannabis abuse or dependence criteria. Dopamine synthesis capacity was negatively associated with higher levels of cannabis use (r = -.77, p < .001) and positively associated with age of onset of cannabis use (r = .51, p = .027) but was not associated with cannabis-induced psychotic-like symptoms (r = .32, p = .19).

Conclusions: These findings indicate that chronic cannabis use is associated with reduced dopamine synthesis capacity and question the hypothesis that cannabis increases the risk of psychotic disorders by inducing the same dopaminergic alterations seen in schizophrenia.

Original languageEnglish
Pages (from-to)470-478
Number of pages9
JournalBiological psychiatry
Volume75
Issue number6
DOIs
Publication statusPublished - 15 Mar 2014

Keywords

  • Addiction
  • dependence
  • dopamine
  • drugs
  • imaging
  • psychosis
  • POSITRON-EMISSION-TOMOGRAPHY
  • SCHIZOPHRENIC-PATIENTS
  • SYNTHESIS CAPACITY
  • INTRAVENOUS DELTA-9-TETRAHYDROCANNABINOL
  • CHRONIC DELTA(9)-TETRAHYDROCANNABINOL
  • RECEPTOR AVAILABILITY
  • BRAIN SYNAPTOSOMES
  • HUMAN STRIATUM
  • YOUNG-ADULTS
  • RAT-BRAIN

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