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Biol Psychiatry. 2016 Jun 15;79(12):997-1005. doi: 10.1016/j.biopsych.2015.08.021. Epub 2015 Aug 29.

Reduced Brain Cannabinoid Receptor Availability in Schizophrenia.

Author information

  • 1Schizophrenia and Neuropharmacology Research Group, Veterans Affairs Connecticut Healthcare System, West Haven; Abraham Ribicoff Research Facilities, Connecticut Mental Health Center, New Haven; Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut. Electronic address: mohini.ranganathan@yale.edu.
  • 2Schizophrenia and Neuropharmacology Research Group, Veterans Affairs Connecticut Healthcare System, West Haven; Abraham Ribicoff Research Facilities, Connecticut Mental Health Center, New Haven; Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut.
  • 3Abraham Ribicoff Research Facilities, Connecticut Mental Health Center, New Haven; Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut; Positron Emission Tomography Center, Yale University School of Medicine, New Haven, Connecticut.
  • 4Positron Emission Tomography Center, Yale University School of Medicine, New Haven, Connecticut.
  • 5Molecular Imaging Program for Mood and Anxiety Disorders, New York University Langone Medical Center, New York, New York.
  • 6Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut.

Abstract

BACKGROUND:

Several lines of evidence suggest the presence of abnormalities in the endocannabinoid (eCB) system in schizophrenia (SCZ). However, there are limited in vivo measures of the eCB system in SCZ.

METHODS:

Twenty five male SCZ subjects (SCZs) (18 antipsychotic treated and 7 antipsychotic free) were compared with 18 age-matched male healthy control subjects (HCs). Subjects underwent one positron emission tomography scan each with the cannabinoid receptor-1 (CB1R) selective radiotracer [(11)C]OMAR on the high resolution research tomography scanner. Regional volume of distribution (VT) values were determined using kinetic modeling of positron emission tomography data as a measure of CB1R availability. Group differences in mean composite [(11)C]OMAR VT values were compared between SCZs and HCs. Exploratory comparisons of CB1R availability within 15 brain regions were also conducted. All analyses were covaried for age and body mass index.

RESULTS:

SCZs showed significantly (p = .02) lower composite [(11)C]OMAR VT relative to HCs (~12% difference, effect size d = .73). [(11)C]OMAR VT was significantly (all ps < .05) lower in SCZs in the amygdala, caudate, posterior cingulate cortex, hippocampus, hypothalamus, and insula. Composite [11]OMAR VT was HCs > antipsychotic treated SZCs > antipsychotic free SZCs. Furthermore, composite [(11)C]OMAR VT was greater in HCs than SCZ smokers (n = 11) and SCZ nonsmokers (n = 14).

CONCLUSIONS:

CB1R availability is lower in male SCZ subjects compared with HCs. Furthermore, antipsychotics and tobacco use may increase CB1R availability in this population. The findings of the study provide further evidence supporting the hypothesis that alterations in the eCB system might contribute to the pathophysiology of SCZ.

KEYWORDS:

Antipsychotics; CB(1)R; Cannabinoid; OMAR; Schizophrenia; Smoking

PMID:
26432420
PMCID:
PMC4884543
[Available on 2017-06-15]
DOI:
10.1016/j.biopsych.2015.08.021
[PubMed - in process]
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