Cannabis cue-induced brain activation correlates with drug craving in limbic and visual salience regions: Preliminary results

Abstract

Craving is a major motivator underlying drug use and relapse but the neural correlates of cannabis craving are not well understood. This study sought to determine whether visual cannabis cues increase cannabis craving and whether cue-induced craving is associated with regional brain activation in cannabis-dependent individuals. Cannabis craving was assessed in 16 cannabis-dependent adult volunteers while they viewed cannabis cues during a functional MRI (fMRI) scan. The Marijuana Craving Questionnaire was administered immediately before and after each of three cannabis cue-exposure fMRI runs. FMRI blood-oxygenation-level-dependent (BOLD) signal intensity was determined in regions activated by cannabis cues to examine the relationship of regional brain activation to cannabis craving. Craving scores increased significantly following exposure to visual cannabis cues. Visual cues activated multiple brain regions, including inferior orbital frontal cortex, posterior cingulate gyrus, parahippocampal gyrus, hippocampus, amygdala, superior temporal pole, and occipital cortex. Craving scores at baseline and at the end of all three runs were significantly correlated with brain activation during the first fMRI run only, in the limbic system (including amygdala and hippocampus) and paralimbic system (superior temporal pole), and visual regions (occipital cortex). Cannabis cues increased craving in cannabis-dependent individuals and this increase was associated with activation in the limbic, paralimbic, and visual systems during the first fMRI run, but not subsequent fMRI runs. These results suggest that these regions may mediate visually cued aspects of drug craving. This study provides preliminary evidence for the neural basis of cue-induced cannabis craving and suggests possible neural targets for interventions targeted at treating cannabis dependence.

Mechanisms Underlying Sex Differences in Cannabis Use

“…Cannabis cue-induced craving has been reported in both men and women [128]. Further, in a mostly female sample of cannabis users, cue-induced craving was correlated with occipital cortex, parahippocampal gyrus, thalamus, hippocampus, superior temporal pole, and middle occipital gyrus activation [129]; however, within-group gender differences were not reported. In women, cannabis cue-induced neural activation of bilateral anterior insula and left lateral orbitofrontal cortex positively and negatively correlated with baseline craving, respectively [125].…”

Modeling Causal Relationship Between Brain Regions Within the Drug-Cue Processing Network in Chronic Cocaine Smokers

“…Nine of these 10 ROIs were selected from Jasinska et al (2014) (see sections 3.1-3.2) and they included amygdala (bilateral; Figure 1a (right)), hippocampus ((right) (Figure 1b)), dorsal striatum (bilateral; Figure 1c (right; putamen)), insula (bilateral; Figure 1d (right)), medial frontal cortex (bilateral; Figure 1e (right)), orbital frontal cortex (bilateral; Figure 1f (right)), dorsolateral prefrontal cortex ((left) (Figure 1g)), anterior cingulate cortex (Figure 1h), and ventral striatum ((right) Figure 1i) ( Table 2). As hippocampus and parahippocampal gyrus are a part of the hippocampal complex (Nadel et al, 2003), and activation in both of these regions has been reported in earlier drug cue reactivity studies (Charboneau et al, 2013;Janes et al, 2010b;Langleben et al, 2008), we decided to include the parahippocampal gyrus ((right; anterior division); Figure 1j) as one of the ROIs in our analysis. Altogether, these 10 ROIs encompass the major areas of the brain's mesocorticolimbic and nigrostriatal systems (Jasinska et al, 2014).…”

Modulation of motivational salience processing during the early stages of psychosis

“…Various factors may have influenced our results, such as different neurocognitive characterizations (Rausch et al, 2013) and profiles of psychotic symptoms in the FEP subgroups; underlying gray matter deficits (Pujol et al, 2013); lack of assessment of the affective state and antidepressants used (Eshel and Roiser, 2010), alcohol (Sullivan et al, 2013), nicotine or cannabis (Charboneau et al, 2013). We acknowledge that different interview measures for prodromal symptoms have been developed that assess either attenuated and/or brief limited psychotic symptoms, or cognitive basic symptoms.…”