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Varenicline effects on drinking, craving and neural reward processing among
non-treatment-seeking alcohol-dependent individuals
#MMPMID24647921
Schacht JP
; Anton RF
; Randall PK
; Li X
; Henderson S
; Myrick H
Psychopharmacology (Berl)
2014[Sep]; 231
(18
): 3799-807
PMID24647921
show ga
RATIONALE: The ?4?2 nicotinic acetylcholine receptor partial agonist varenicline
has been reported to reduce drinking among both heavy-drinking smokers and
primary alcoholics, and this effect may be related to varenicline-mediated
reduction of alcohol craving. Among smokers, varenicline has been reported to
modulate cigarette cue-elicited brain activation in several reward-related areas.
OBJECTIVES: This pilot study tested varenicline's effects on drinking, alcohol
craving, and alcohol cue-elicited activation of reward-related brain areas among
non-treatment-seeking alcohol-dependent individuals. METHODS: Thirty-five such
individuals (mean age?=?30, 57 % male, 76 % heavy drinking days in the past
month, 15 smokers) were randomized to either varenicline (titrated to 2 mg) or
placebo for 14 days, and were administered an alcohol cue reactivity fMRI task on
day 14. A priori regions of interest (ROIs) were bilateral and medial
orbitofrontal cortex (OFC), right ventral striatum (VS), and medial prefrontal
cortex (mPFC). RESULTS: Despite good medication adherence, varenicline did not
reduce heavy drinking days or other drinking parameters. It did, however,
increase self-reported control over alcohol-related thoughts and reduced
cue-elicited activation bilaterally in the OFC, but not in other brain areas.
CONCLUSIONS: These data indicate that varenicline reduces alcohol craving and
some of the neural substrates of alcohol cue reactivity. However, varenicline
effects on drinking mediated by cue-elicited brain activation and craving might
be best observed among treatment-seekers motivated to reduce their alcohol
consumption.
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