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Introduction: Virtual reality (VR) has been shown to be effective in eliciting responses to nicotine cues in cigarette smokers. The primary aim of this study was to investigate whether cigarette-deprived smokers would exhibit increased craving and changes in heart rate when viewing cigarette related cues as compared to non-smoking cues in a VR environment, and the secondary aim was to assess the extent to which self-assessed measures of withdrawal and dependence correlated with VR craving. Methods: Nicotine-dependent cigarette smokers were recruited for a 2 day study. On Day 1, participants smoked as usual and on Day 2 were deprived from smoking overnight. On both days, participants completed self-assessment questionnaires on withdrawal, craving, and nicotine-dependence. Participants completed a VR session during the cigarette deprivation condition only (Day 2). During this session, they were exposed to active smoking and placebo (non-smoking) cues. Results: The data show that self-reported levels of “craving” (p < .01) and “thinking about cigarettes” (p < .0001) were significantly greater after exposure to the active cues versus non-smoking cues. Significant increases in heart rate were found for 3 of 4 active cues when compared to non-smoking cues (p < .05). Finally, significant positive correlations were found between self-reported craving prior to the VR session and craving induced by active VR cues (p < .01). Conclusions: In this report, active VR cues elicited craving during cigarette deprivation. This is the first study to demonstrate that self-reported craving, withdrawal symptoms, and nicotine dependence severity predict cue-induced craving in the VR setting.

Background: Cholinergic transmission is altered by drugs of abuse and contributes to psychostimulant reinforcement. In particular, acetylcholinesterase inhibitors, like huperzine A, may be effective as treatments for cocaine use disorder. Methods: The current report describes results from a double-blind, placebo-controlled study in which participants (n=14–17/group) were randomized to huperzine A (0.4 or 0.8mg) or placebo. Participants received randomized infusions of cocaine (0 and 40mg, IV) on days 1 and 9. On day 10, participants received noncontingent, randomized infusions of cocaine (0 and 20mg, IV) before making 5 choices to receive additional infusions. Results: Huperzine A was safe and well-tolerated and compared with placebo, treatment with huperzine A did not cause significant changes in any cocaine pharmacokinetic parameters (all P >.05). Time-course and peak effects analyses show that treatment with 0.4mg of huperzine A significantly attenuated cocaine-induced increases of “Any Drug Effect,” “High,” “Stimulated,” “Willing to Pay,” and “Bad Effects” (all P >.05). Conclusions: The current study represents a significant contribution to the addiction field since it serves as the first published report on the safety and potential efficacy of huperzine A as a treatment for cocaine use disorder.

A variety of neuropharmacological strategies are being pursued in the search for an effective treatment for methamphetamine addiction. In this study, we investigated the safety and potential efficacy of aripiprazole, an antipsychotic agent acting on both dopamine and serotonin systems. We conducted a double-blind inpatient clinical pharmacology study to assess potential interactions between intravenous (IV) methamphetamine (15mg and 30mg) and oral aripiprazole (15mg). In addition, the effects of aripiprazole treatment on abstinence related craving and cue-induced craving were evaluated. Participants included non-treatment seeking, methamphetamine dependent patients (N=16), 18-45 years of age, currently using methamphetamine. Following baseline methamphetamine dosing (15mg and 30mg), participants received 2 weeks of treatment with aripiprazole (n=8) or placebo (n=8). Participants then completed cue exposure sessions using neutral and methamphetamine-related cues. Methamphetamine dosing (15mg and 30mg) was then repeated. Aripiprazole treatment had no effect on cue-induced methamphetamine craving, or on daily baseline craving assessed over the course of medication treatment, though aripiprazole treatment was associated with increased craving independent of methamphetamine dosing. Aripiprazole treatment was associated with significantly higher ratings on ARCI subscales reflecting euphoria and amphetamine-like effects following methamphetamine dosing. Aripiprazole was treatment was also associated with significant reductions in ratings of “bad effects” and reductions on the ARCI subscale for sedation effects following methamphetamine dosing. Aripiprazole treatment reduced the increase in systolic blood pressure following methamphetamine dosing, but had no other effects on cardiovascular responses to methamphetamine. Aripiprazole treatment did not alter the pharmacokinetics of methamphetamine. These findings indicate that aripiprazole treatment appears to be safe in volunteers with methamphetamine dependence, though the finding that aripiprazole increased some of the rewarding and stimulatory effects produced by acute methamphetamine suggests that 15mg aripiprazole is unlikely to be efficacious for the treatment of methamphetamine dependence. Further research with lower doses of aripiprazole, possibly using study designs aimed at evaluating efficacy for relapse prevention, are needed before ruling out aripiprazole as a treatment for methamphetamine dependence.