Identifying neural signatures of tobacco retail outlet exposure: Preliminary validation of a "community neuroscience" paradigm.

An extensive epidemiological literature indicates that increased exposure to tobacco retail outlets (TROs) places never smokers at greater risk for smoking uptake and current smokers at greater risk for increased consumption and smoking relapse. Yet research into the mechanisms underlying this effect has been limited. This preliminary study represents the first effort to examine the neurobiological consequences of exposure to personally relevant TROs among both smokers (n = 17) and nonsmokers (n = 17). Individuals carried a global positioning system (GPS) tracker for 2 weeks. Traces were used to identify TROs and control outlets that fell inside and outside their ideographically defined activity space. Participants underwent functional MRI (fMRI) scanning during which they were presented with images of these storefronts, along with similar store images from a different county and rated their familiarity with these stores. The main effect of activity space was additive with a Smoking status × Store type interaction, resulting in smokers exhibiting greater neural activation to TROs falling inside activity space within the parahippocampus, precuneus, medial prefrontal cortex, and dorsal anterior insula. A similar pattern was observed for familiarity ratings. Together, these preliminary findings suggest that the otherwise distinct neural systems involved in self-orientation/self-relevance and smoking motivation may act in concert and underlie TRO influence on smoking behavior. This study also offers a novel methodological framework for evaluating the influence of community features on neural activity that can be readily adapted to study other health behaviors.

Review of Popularity and Quality Standards of Opioid-Related Smartphone Apps.

PURPOSE OF REVIEW: Opioid misuse, addiction, and related harm is a global crisis that affects public health and social and economic welfare. Many of the strategies being used to combat the opioid crisis could benefit from improved access and dissemination, such as that afforded by smartphone apps. The goal of this study was to characterize the purpose, audience, quality and popularity of opioid-related smartphone apps. Using web scraping, available information from 619 opioid-related apps (e.g., popularity metrics) was downloaded from Google Play, and 59 apps met criteria for review. The apps were additionally coded for quality by two raters using an 8-item screener for the American Psychiatric Association App Evaluation Model. FINDINGS: Sixty one percent of apps targeted patients, 29% providers, 8% the general community, and 2% healthcare trainees. Regarding app purpose, 49% addressed treatment, 27% prevention, and 24% overdose. Only one app met all criteria on the screener for quality, and there was no association between a total score calculated for the screener and measures of app popularity (e.g., star ratings; R2=0.10, p=0.19). SUMMARY: Opioid-related apps available for consumers addressed key stakeholders (patients, providers, community) and were consistent with strategies to address the opioid crisis (prevention, treatment, overdose). However, there was little evidence that available opioid-related apps meet basic quality standards, and no relationship was found between app quality and popularity. This review was conducted at the level of consumer decision-making (i.e., the app store), where only a handful of opioid-related apps met quality standards enough to warrant a more detailed evaluation of the app before recommendation for use. Because smartphone apps could be a critical tool to increase access to and utilization of opioid prevention, treatment, and recovery services, further development and testing is sorely needed.

The effects of nicotine and non-nicotine smoking factors on working memory and associated brain function.

Smoking abstinence impairs executive function, which may promote continued smoking behavior and relapse. The differential influence of nicotine and non-nicotine (i.e. sensory, motor) smoking factors and related neural substrates is not known. In a fully factorial, within-subjects design, 33 smokers underwent fMRI scanning following 24 hours of wearing a nicotine or placebo patch while smoking very low nicotine content cigarettes or remaining abstinent from smoking. During scanning, blood oxygenation level-dependent (BOLD) signal was acquired while participants performed a verbal N-back task. Following 24-hour placebo (versus nicotine) administration, accuracy on the N-back task was significantly worse and task-related BOLD signal lower in dorsomedial frontal cortex. These effects were observed irrespective of smoking. Our data provide novel evidence that abstinence-induced deficits in working memory and changes in underlying brain function are due in large part to abstinence from nicotine compared with non-nicotine factors. This work has implications both for designing interventions that target abstinence-induced cognitive deficits and for nicotine-reduction policy.

Association between the oxytocin receptor (OXTR) gene and mesolimbic responses to rewards.

BACKGROUND: There has been significant progress in identifying genes that confer risk for autism spectrum disorders (ASDs). However, the heterogeneity of symptom presentation in ASDs impedes the detection of ASD risk genes. One approach to understanding genetic influences on ASD symptom expression is to evaluate relations between variants of ASD candidate genes and neural endophenotypes in unaffected samples. Allelic variations in the oxytocin receptor (OXTR) gene confer small but significant risk for ASDs for which the underlying mechanisms may involve associations between variability in oxytocin signaling pathways and neural response to rewards. The purpose of this preliminary study was to investigate the influence of allelic variability in the OXTR gene on neural responses to monetary rewards in healthy adults using functional magnetic resonance imaging (fMRI). METHODS: The moderating effects of three single nucleotide polymorphisms (SNPs) (rs1042778, rs2268493 and rs237887) of the OXTR gene on mesolimbic responses to rewards were evaluated using a monetary incentive delay fMRI task. RESULTS: T homozygotes of the rs2268493 SNP demonstrated relatively decreased activation in mesolimbic reward circuitry (including the nucleus accumbens, amygdala, insula, thalamus and prefrontal cortical regions) during the anticipation of rewards but not during the outcome phase of the task. Allelic variation of the rs1042778 and rs237887 SNPs did not moderate mesolimbic activation during either reward anticipation or outcomes. CONCLUSIONS: This preliminary study suggests that the OXTR SNP rs2268493, which has been previously identified as an ASD risk gene, moderates mesolimbic responses during reward anticipation. Given previous findings of decreased mesolimbic activation during reward anticipation in ASD, the present results suggest that OXTR may confer ASD risk via influences on the neural systems that support reward anticipation.

Smoking withdrawal in smokers with and without posttraumatic stress disorder.

INTRODUCTION: Previous research on smoking withdrawal in posttraumatic stress disorder (PTSD) has been limited by the use of retrospective and observational methods and has lacked repeated assessments on the first day of abstinence and evaluation of the conditioned effects of smoking. METHODS: Smokers with (n = 17; 59% female) and without (n = 30; 17% female) PTSD completed 3 randomly ordered experimental sessions using a 2 (group: PTSD vs. non-PTSD) × 3 (smoking condition: usual brand vs. nicotine free vs. no smoking) design. Before the smoking manipulation, participants completed self-report measures of smoking urges and withdrawal, followed by withdrawal assessment after the smoking manipulation. RESULTS: Compared with smokers without PTSD, smokers with PTSD exhibited higher craving (χ1² = 16.60, p < .001) and habit withdrawal (χ1² = 10.38, p = .001) following overnight abstinence. PTSD smokers also exhibited worsening negative affect throughout the morning when not smoking a cigarette (χ1² = 11.30, p = .004). After smoking, smokers with PTSD reported diminished relief from craving (χ1² = 6.49, p = .011), negative affect (χ1² = 4.51, p = .034), arousal (χ1² = 6.46, p = .011), and habit withdrawal (χ1² = 7.22, p = .007), relative to smokers without PTSD. CONCLUSIONS: Results of this preliminary investigation suggested that after overnight abstinence, PTSD smokers experienced worse withdrawal symptoms and greater urges to smoke for both positive and negative reinforcement. Research on smoking withdrawal early in the course of smoking abstinence in PTSD could inform interventions targeting abstinence early in the quit attempt.

ADHD and smoking: from genes to brain to behavior.

Attention-deficit/hyperactivity disorder (ADHD) and tobacco smoking are among the most common and costly psychiatric and behavioral problems. The rates of co-occurrence of these two common problems are larger than expected by chance. Despite progress in identifying the neural and genetic substrates of each, the mechanisms underlying the high rates of comorbidity between ADHD and smoking remain largely unknown. We propose that ADHD and smoking involve dysregulation of dopaminergic and nicotinic-acetylcholinergic circuits and that these aberrations are likely to arise, at least in part, from genetic variations. This review describes an integrative model of the ADHD-smoking comorbidity, with an emphasis on shared neuropharmacological mechanisms. We first describe the prevalence of smoking among ADHD patients. We then describe how ADHD influences stages of smoking behavior (e.g., initiation, maintenance, and relapse). We review common potential genetic substrates of ADHD and smoking, focusing on genes that regulate monoaminergic neurotransmission. We review the behavioral and neuropharmacological bases of smoking and ADHD, focusing on the modulatory roles of nicotine on attention and behavioral control. Finally, we discuss the implications of this model for prevention and clinical outcomes.