Smoking Progression and Nicotine-Enhanced Reward Sensitivity Predicted by Resting-State Functional Connectivity in Salience and Executive Control Networks.

INTRODUCTION: The neural underpinnings underlying individual differences in nicotine-enhanced reward sensitivity and smoking progression are poorly understood. Thus, we investigated whether brain resting-state functional connectivity (rsFC) during smoking abstinence predicts nicotine-enhanced reward sensitivity and smoking progression in young light smokers. We hypothesized that high rsFC between brain areas with high densities of nicotinic receptors (insula, anterior cingulate cortex [ACC], hippocampus, thalamus) and areas involved in reward-seeking (nucleus accumbens [NAcc], prefrontal cortex [PFC]) would predict nicotine-enhanced reward sensitivity and smoking progression. METHODS: Young light smokers (N=64, age 18-24, M = 1.89 cigarettes/day) participated in the study. These individuals smoked between 5 to 35 cigarettes per week and lifetime use never exceeded 35 cigarettes per week. Their rsFC was assessed using functional magnetic resonance imaging after 14-hour nicotine-deprivation. Subjects also completed a probabilistic reward task after smoking a placebo on one day and a regular cigarette on another day. RESULTS: The probabilistic-reward-task assessed greater nicotine-enhanced reward sensitivity was associated with greater rsFC between the right anterior PFC and right NAcc, but with reduced rsFC between the ACC and left inferior prefrontal gyrus and the insula and ACC. Decreased rsFC within the salience network (ACC and insula) predicted increased smoking progression across 18 months and greater nicotine-enhanced reward sensitivity. CONCLUSIONS: These findings provide the first evidence that differences in rsFCs in young light smokers are associated with nicotine-enhanced reward sensitivity and smoking progression. IMPLICATIONS: Weaker rsFC within the salience network predicted greater nicotine-enhanced reward sensitivity and smoking progression. These findings suggest that salience network rsFC and drug-enhanced reward sensitivity may be useful tools and potential endophenotypes for reward sensitivity and drug-dependence research.

Effects of nicotine patches on early and late attentional bias to smoking cues: We may know less than we think.

In contrast to overnight deprivation versus satiety studies, a small number of placebo-controlled studies have failed to find that nicotine administration reduces attentional bias (AB) to smoking cues. To assess the reliability of this failure and to address the duration and salience of AB in smokers versus never-smokers, we used a longer-than-typical (i.e., 3,000 ms) smoking cue-presentation time in a placebo-controlled trial of smokers and never-smokers. We aimed to assess whether a nicotine patch (i.e., active vs. placebo) attenuates continuously assessed eye gaze-measured AB to smoking cues across 3,000 ms in 32 habitual, overnight-deprived smokers and smoker-nonsmoker differences compared to 32 never-smokers. We presented a series of picture pairs (i.e., one smoking-related and one affectively neutral control picture) simultaneously to assess AB. Participants attended a 14 mg nicotine patch and a placebo patch session in a randomized order. The habitual smokers were 12-18 hr nicotine-deprived during both sessions. Smokers demonstrated a stronger AB toward smoking cues than never-smokers across the entire 3,000 ms cue-presentation time. Nicotine did not significantly reduce the AB to smoking cues but the AB was strongly and positively related to deprivation-associated cravings in smokers. Patch-delivered nicotine did not reduce AB to smoking cues presented for up to 3,000 ms, even though smoker-nonsmoker differences in bias remained. Assessments of longer cue presentations and more subtle cues may provide nuance not currently captured by existing studies, because of potential demand effects in designs that contrast overnight versus sated state effects on AB. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Facilitated extinction of conditioned fear responses by delta 9-tetrahyrdrocannabidol in humans: a pilot study.

OBJECTIVE: We sought to determine whether acute delta 9-tetrahyrdrocannabidol (THC) administration would facilitate fear extinction in young occasional cannabis users, given that animal models indicate THC facilitates extinction learning, and recent studies indicate THC administration may also enhance threat memory extinction in humans. METHODS: On each of the 2 days, 24+ hour THC-deprived participants were conditioned to fear visual stimuli in a delay conditioning and extinction paradigm. Both CS+ and CS- were faces of negative emotional valence, with the CS+ paired with mild electric shock. Throughout both conditioning and extinction paradigms, EEG was measured to quantify event-related potentials for these learning processes. Following conditioning, individuals, in a randomized and counter-balanced order, smoked either an active THC cigarette (26.25 mg/2.7% THC) or a placebo marijuana cigarette (0.002% THC) on 1 day and the opposite cigarette on the second day. After smoking, CS+ and CS- were presented without shock, resulting in extinction of conditioned fear. RESULTS: Relative to placebo, THC facilitated extinction of the conditioned response to the CS+, as reflected by reductions in late positive potential amplitude during extinction learning. CONCLUSIONS: The results indicate that acute THC administration may facilitate extinction of the conditioned fear response in humans.

Anhedonia in Nicotine Dependence.

Prior findings indicate that trait anhedonia enhances the likelihood of becoming a tobacco smoker, and preliminary evidence suggests that smoking abstinence leads to anhedonic states in some individuals and situations, and nicotine administration reduces anhedonic states. Nevertheless, many vital questions exist concerning relationships between anhedonia and nicotine dependence, including situational and individual difference factors that may moderate the strength of these associations. This chapter provides a critical review of the literature assessing relationships of anhedonia to nicotine dependence and the effects of acute nicotine through the lenses of the Research Domain Criteria's (RDoC) Positive Valence Systems (NIMH, RDoC changes to the matrix (CMAT) workgroup update: proposed positive valence domain revisions. A report by the national advisory mental health council workgroup on changes to the research domain criteria matrix, 2018) and the Situation x Trait Affective Response (STAR) model of nicotine's effects and nicotine dependence (Gilbert, Smoking individual differences, psychopathology, and emotion. Taylor and Francis, Washington, DC, 1995; Gilbert, Hum Psychopharmacol Clin Exp 12:S89-S102, 1997). The effects of nicotine and nicotine withdrawal on subjective, behavioral, and brain indices vary across the three RDoC Positive Valences Systems (Reward Responsiveness, Reward Learning, and Reward Valuation) in a manner that supports the research and potential clinical utility of using RDoC criteria and the STAR model to guide research and clinical innovation. We provide a revision of the STAR model that incorporates the three RDoC Positive Valence Systems with evidence that nicotine's effects on hedonic and affective processes vary as a function of the dominance/salience of (1) situational hedonic and affective cues and task/active coping cues, and (2) state executive functioning level/capacity and state reward sensitivity such that these effects of nicotine are maximal during states of suboptimal cognitive functioning and reward sensitivity, combined with low situational stimulus salience and low task-related cues/demands.

Effects of Cannabis-Delivered THC on mood and negative attentional bias in the context of positive vs. neutral Alternatives-a pilot study.

OBJECTIVE: To assess: (1) the acute effects of smoked marijuana (MJ) on negative attentional bias (NAB), (2) moderation of these effects by positive versus neutral alternatives, and (3) the associations of tetrahydrocannabinol (THC)-induced changes in NAB with changes in affect. METHODS: Fourteen MJ users (1-4 uses/wk) smoked a THC cigarette on 1 day and a placebo cigarette on the other counterbalanced day. After smoking, participants freely gazed back and forth at a series of two side-by-side pictures pairs presented for 3000 ms (one negative, while the other was either positive or neutral) while eye gaze was tracked. RESULTS: The effects of THC relative to placebo varied across time such that THC increased NAB during the early temporal component of threatening picture viewing, 333-858 ms after dual-picture onset, regardless of alternative picture valance. However, contrary to the attentional bias-causes affect hypothesis, during the early viewing phase THC-enhanced positive affect (PA) correlated positively with THC-induced NAB. In contrast, during the late phase (891-3000 ms) THC-enhanced PA did not correlate significantly with NAB, though THC-induced negative affect (NA) change did correlate positively with THC-induced change in NAB in the positive alternative condition. CONCLUSIONS: We replicated findings of others showing that THC can enhance NAB during the early stages of threatening picture viewing. We extended previous results by demonstrating the THC-induced NAB is associated with increased PA during initial threat viewing, but with increased NA during later processing if positive alternatives are present.

Genetic and Depressive Traits Moderate the Reward-Enhancing Effects of Acute Nicotine in Young Light Smokers.

INTRODUCTION: Rates of light smoking have increased in recent years and are associated with adverse health outcomes. Reducing light smoking is a challenge because it is unclear why some but not others, progress to heavier smoking. Nicotine has profound effects on brain reward systems and individual differences in nicotine's reward-enhancing effects may drive variability in smoking trajectories. Therefore, we examined whether a genetic risk factor and personality traits known to moderate reward processing, also moderate the reward-enhancing effects of nicotine. METHODS: Light smokers (n = 116) performed a Probabilistic Reward Task to assess reward responsiveness after receiving nicotine or placebo (order counterbalanced). Individuals were classified as nicotine dependence 'risk' allele carriers (rs16969968 A-allele carriers) or non-carriers (non-A-allele carriers), and self-reported negative affective traits were also measured. RESULTS: Across the sample, reward responsiveness was greater following nicotine compared to placebo (p = 0.045). For Caucasian A-allele carriers but not non-A-allele carriers, nicotine enhanced reward responsiveness compared to placebo for those who received placebo first (p = 0.010). Furthermore, for A-allele carriers but not non-A-allele carriers who received nicotine first, the enhanced reward responsiveness in the nicotine condition carried over to the placebo condition (p < 0.001). Depressive traits also moderated the reward-enhancing effects of nicotine (p = 0.010) and were associated with blunted reward responsiveness following placebo but enhanced reward responsiveness following nicotine. CONCLUSION: These findings suggest that individual differences in a genetic risk factor and depressive traits alter nicotine's effect on reward responsiveness in light smokers and may be important factors underpinning variability in smoking trajectories in this growing population. IMPLICATIONS: Individuals carrying genetic risk factors associated with nicotine dependence(rs16969968 A-allele carriers) and those with higher levels of depressive personality traits, showmore pronounced increases in reward learning following acute nicotine exposure. These findingssuggest that genetic and personality factors may drive individual differences in smoking trajectoriesin young light smokers by altering the degree to which nicotine enhances reward processing. CLINICAL TRIAL REGISTRATION: NCT02129387 (pre-registered hypothesis: www.clinicaltrials.gov).

APOE genotype influences P3b amplitude and response to smoking abstinence in young adults.

RATIONALE: There is strong evidence that nicotine can enhance cognitive functions and growing evidence that this effect may be larger in young healthy APOE ε4 carriers. However, the moderating effects of the APOE ε4 allele on cognitive impairments caused by nicotine deprivation in chronic smokers have not yet been studied with brain indices. OBJECTIVE: We sought to determine whether young female carriers of the APOE ε4 allele, relative to noncarriers, would exhibit larger abstinence-induced decreases in P3b amplitude during a two-stimulus auditory oddball task. METHODS: We compared parietal P3bs in female chronic smokers with either APOE ε3/ε3 (n = 54) or ε3/ε4 (n = 20) genotype under nicotine-sated conditions and after 12-17-h nicotine deprivation. RESULTS: Nicotine deprivation significantly reduced P3b amplitudes in APOE ε4 carriers, but not in APOE-ε3/ε3 individuals, such that the difference seen prior to nicotine deprivation was eliminated. CONCLUSIONS: The results suggest that subjects with the APOE ε4 allele are more sensitive to nicotine, which could influence smoking patterns, the risk for nicotine dependence, and the cognitive effects of nicotine use in these individuals.

Depression and Nicotine Withdrawal Associations with Combustible and Electronic Cigarette Use.

Depression is a risk factor for nicotine use and withdrawal. Population level epidemiologic studies that include users of either combustible or electronic cigarette (NICUSER) could inform interventions to reduce nicotine dependence in vulnerable populations. The current study examined the relationship between depression diagnosis (DEPDX), NICUSER, and lifetime rates of DSM-V nicotine withdrawal (NW) symptoms in a nationally representative sample of US adults (N = 979), who answered related questions in surveys administered through GfK's KnowledgePanel. Over 42% of the sample reported lifetime ever combustible cigarette use, 15.6% electronic-cigarette use, and 45.9% either (NICUSER). Weighted logistic regression analyses (controlling for age and gender) found that DEPDX was associated with 2.3 times increased odds (ratio (OR); 95% Confidence Interval (CI): 1.5-3.5) of being a NICUSER. Regarding risks of NW symptoms among NICUSER, models that additionally controlled for frequency of nicotine use found that DEPDX was significantly associated with increased odds of concentration problems (OR = 2.4; 95% CI: 1.3-4.5) and depressed mood (OR = 2.2; 95% CI: 1.1-4.1) when quitting or cutting down on nicotine use. Results highlight the consistent comorbidity between depression, nicotine use, and symptomatic nicotine withdrawal in a population-based sample of combustible and electronic cigarette users.

Nicotine patch for cannabis withdrawal symptom relief: a randomized controlled trial.

RATIONALE: Given that tetrahydrocannabinol (THC) and nicotine have similar effects on negative affect (NA), we hypothesized that a 7-mg nicotine patch (NP) would reduce NA-related cannabis (CAN) withdrawal symptoms in cannabis-dependent (CD) individuals who were not nicotine dependent. OBJECTIVE: We sought to determine whether NP reduces NA across 15 days of CAN abstinence in two groups: non-tobacco smokers (NTS) and light tobacco smokers (LTS). METHODS: CD participants (N = 127; aged 18-35) who used CAN at least 5 times/week for the past 12 + months were randomized to (1) NP or (2) a placebo patch (PP) and received $300 for sustained biochemically verified CAN abstinence. Of those randomly assigned, 52 of 63 NP, and 56 of 64 PP maintained biochemically verified CAN abstinence and 51 NP and 50 PP participants complied with all aspects of the study. Affect and other withdrawal symptoms were measured every 48 h across 15 days of CAN abstinence. RESULTS: After controlling for age, tobacco use, baseline THC concentration, and baseline measurements of the dependent variable, NP reduced NA symptoms across the 15-day treatment relative to PP. Differences in NA and CAN withdrawal symptoms were not moderated by tobacco user status. CONCLUSIONS: The findings provide the first evidence that NP may be able to attenuate NA-related withdrawal symptoms in individuals with cannabis use disorder who are not heavy users of tobacco or nicotine. CLINICAL TRIALS REGISTRY: NCT01400243 http://www.clinicaltrials.gov.

The impact of nicotine dose and instructed dose on smokers' implicit attitudes to smoking cues: An ERP study.

It is unclear whether nicotine and perceived nicotine exposure can influence automatic evaluations of cigarette stimuli. In the present study, we investigated the effects of nicotine dose and instructed dose on motivational responses to smoking cues. Forty overnight nicotine-deprived smokers completed an Implicit Association Test (IAT) at each of the four laboratory sessions in a balanced-placebo design that crossed nicotine dose (Given-NIC [given nicotine] vs. Given-DENIC [given denicotinized]) with instructed dose expectancy (Told-NIC [told-nicotine] vs. Told-DENIC. [told-denicotinized]). We measured participants' behavioral performance, including reaction time (RT) and accuracy rate, and the early posterior negativity (EPN) component using the event-related potential (ERP) technique to the target pictures. During congruent trials when the categorization condition was smoking or unpleasant, smokers had greater classification accuracy, shorter RT latency, and greater EPN amplitudes compared to the incongruent trials when the categorization condition was smoking or pleasant. The Given-NIC condition was associated with increased classification accuracy, longer RT latency, and decreased EPN amplitudes compared to the Given-DENIC condition. Similarly, the Told-NIC condition was associated with increased accuracy and decreased EPN amplitudes compared to the Told-DENIC condition, but with shorter RT latency. Cigarette-related pictures produced greater EPN amplitudes than neutral pictures. Both behavioral and ERP results suggest that smokers have negative implicit attitudes toward smoking. While both nicotine dose and expected dose facilitated stimulus categorization, there was no evidence that either factor altered smokers' negative attitudes toward smoking cues. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Smoking abstinence symptoms across 67 days compared with randomized controls-Moderation by nicotine replacement therapy, bupropion, and negative-affect traits.

Accurate knowledge of negative affect (NA)-related smoking abstinence symptoms (SAS) severity and duration and their moderation by pharmacotherapy and NA-related personality traits is critical for efficacious treatments given that elevated state and trait NA are predictors of relapse. However, SAS severity, duration, and moderation are not well characterized. To date, the longest randomized controlled trial (RCT) of NA-related SAS using randomized delayed-quit smoking controls only examined symptoms across 45 days, despite clinical evidence that SAS may last longer. The present RCT assessed SAS across 67 days in dependent smokers (N = 95) who were randomized either to quit or to delay quitting for the course of the trial. The quit group was further randomized to receive either nicotine replacement therapy (NRT), bupropion (BUP), or placebo. Abstinence-related increases in anger-irritability, depressive, anxiety, and general NA symptoms did not resolve relative to the delayed quit group (DQG) levels across the 67 days in any of the 3 quit groups, though craving fell to below DQG and prequit levels. While NRT attenuated Day 3 SAS relative to BUP and placebo, BUP and NRT generally did not reduce SAS. High scores on trait measures of NA/neuroticism predicted greater increases in and duration of NA-related SAS, potentially indicating that smoking abstinence unmasks affective symptoms. Positive affect was not impacted by abstinence or treatment. The results support the views that (a) prequit baseline values are not a valid index of NA SAS recovery, and (b) on average, NA-related SAS take longer than 67 days to resolve. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Effects of bupropion sustained release on task-related EEG alpha activity in smokers: Individual differences in drug response.

The mechanisms underlying bupropion's efficacy as an antidepressant and a smoking cessation aid are far from being fully characterized. The present study is the first to examine the effects of bupropion on visuospatial task-related parietal EEG alpha power asymmetry-an asymmetry that has previously been found to be associated with severity of depressive symptoms (i.e., the more depressive symptoms, the greater alpha power in the right vs. left parietal area [Henriques & Davidson, 1997; Rabe, Debener, Brocke, & Beauducel, 2005]). Participants, all of whom were smokers and none of whom were clinically depressed, were randomly assigned to the Placebo group (n = 79) or Bupropion group (n = 31) in a double-blind study. EEG during the performance of the visuospatial task was collected before and after 14 days on placebo or bupropion sustained-release capsules. Relative to the Placebo group, the Bupropion group (especially, the Bupropion subgroup who had a positive right versus left parietal alpha power asymmetry at pretreatment) had a reduction in the parietal alpha asymmetry (driven largely by a decrease in right parietal alpha power). These findings support the hypothesis that bupropion can induce changes in parietal EEG asymmetry that have been shown in previous literature to be associated with a reduction in depressive states and traits. (PsycINFO Database Record

Negative affect subtypes and craving differentially predict long-term cessation success among smokers achieving initial abstinence.

OBJECTIVE: This study aimed to examine the associations of individual trajectories of three types of negative affect (NA: anxiety, depression, and anger) and craving during a 44-day period of incentivized smoking abstinence period with cessation outcome at 3 months and at 1 year. METHODS: Adult smokers (N = 140) completed questionnaire assessments of NA and craving during pre-quit baseline sessions and 15 postquit sessions over the 45 days of biochemically verified abstinence while on nicotine or placebo patch treatment. Growth curve and logistic regression analyses were used to examine the associations of trajectory parameters of the individual NA states and craving with the abstinence outcomes at 3 months and 1 year postquit. RESULTS: Greater declines in anxiety, depression, and anger symptoms over the first 44 days of smoking cessation were predictive of higher odds of abstinence at both 3 months and 1 year. Moreover, the greater declines in anxiety and anger remained as significant predictors of abstinence at both time points, independent of the predictive ability of the trajectory profiles of craving. CONCLUSIONS: The findings suggest that slower dissipation of NA, especially anxiety and anger, represents a greater risk for relapse to smoking beyond that predicted by craving during early abstinence. Thus, temporal profiles of the affective symptoms convey unique motivational significance in relapse. Reduction in NA during early abstinence may be a valid target for interventions to increase long-term cessation success rates particularly among individuals with refractory affective symptoms.

Moderation of nicotine effects on covert orienting of attention tasks by poor placebo performance and cue validity.

INTRODUCTION AND RATIONALE: Given baseline-dependent effects of nicotine on other forms of attention, there is reason to believe that inconsistent findings for the effects of nicotine on attentional orienting may be partly due to individual differences in baseline (abstinence state) functioning. Individuals with low baseline attention may benefit more from nicotine replacement. METHOD: The effects of nicotine as a function of baseline performance (bottom, middle, and top third of mean reaction times during placebo) were assessed in 52 habitual abstinent smokers (26 females/26 males) utilizing an arrow-cued covert orienting of attention task. RESULTS: Compared to a placebo patch, a 14mg nicotine patch produced faster overall reaction times (RTs). In addition, individuals with slower RTs during the placebo condition benefitted more from nicotine on cued trials than did those who had shorter (faster) RTs during placebo. Nicotine also enhanced the validity effect (shorter RTs to validly vs. invalidly cued targets), but this nicotine benefit did not differ as a function of overall placebo-baseline performance. CONCLUSIONS: These findings support the view that nicotine enhances cued spatial attentional orienting in individuals who have slower RTs during placebo (nicotine-free) conditions; however, baseline-dependent effects may not generalize to all aspects of spatial attention. These findings are consistent with findings indicating that nicotine's effects vary as a function of task parameters rather than simple RT speeding or cognitive enhancement.

Attentional bias to smoking and other motivationally relevant cues is affected by nicotine exposure and dose expectancy.

We investigated the effects of acute nicotine dose and expected dose on attentional bias (AB) to smoking and affective cues in overnight nicotine-deprived smokers (n=51; 24 women) using a balanced placebo design, which counterbalanced given nicotine dose (Given-NIC vs. Given-DENIC) with instructed nicotine dose expectancy (Told-NIC vs. Told-DENIC). Before and after smoking a study cigarette, smokers completed a vigilance task where they pressed buttons to every third consecutive even or odd digit, while ignoring intermittent smoking, pleasant, unpleasant, and neutral picture distracters. We examined the early posterior negativity (EPN) and late positive potential (LPP) components of the event-related potentials (ERPs) to the distracters, reaction time (RT) to the target digits, and ratings of the study cigarettes. The EPN was sensitive to both given and instructed nicotine dose, while the instructed dose moderated the impact of given dose for the LPP. The RT metrics were sensitive to given but not to instructed dose. The effects of given dose on ratings following cigarette smoking (e.g. enjoyment) were moderated by the instructed dose. The ERP findings suggest that the anticipated effects of nicotine improve attention much like receiving actual nicotine.

The effects of nicotine dose expectancy and motivationally relevant distracters on vigilance.

The imminence of drug use (i.e., drug availability) has been found to be related to intensity of drug craving, but its effects on attentional bias to drug cues are unclear. This study investigated the effects of nicotine availability on attentional bias to smoking, affective, and neutral cues in a sample of adult smokers during a vigilance task. At the beginning of each of 4 laboratory sessions, overnight nicotine-deprived smokers (n = 51) were instructed that they would smoke a cigarette containing either nicotine (Told-NIC) or no nicotine (Told-DENIC) after completing the rapid visual information processing task with central emotional distracters (RVIP-CED). The RVIP-CED presented digits at a rapid pace, with participants instructed to respond with button presses to every third consecutive even or odd digit. Some digits were preceded by smoking, pleasant, unpleasant, or neutral distracter slides. During Told-NIC conditions, participants produced significantly longer reaction time (RT) latency than during Told-DENIC conditions. RT sensitivity (d'), a measure of the ability to discriminate true positives from false positives, was significantly lower during the Told-NIC than during the Told-DENIC conditions to targets following cigarette distracters. These results suggest that nicotine-deprived smokers expecting to imminently smoke a cigarette experience greater distraction, particularly to smoking-related stimuli, than when expecting to smoke a denicotinized cigarette.

Effects of nicotine on emotional distraction of attentional orienting: evidence of possible moderation by dopamine type 2 receptor genotype.

INTRODUCTION: Growing evidence suggests that attentional bias to, and distraction by, emotional stimuli may moderate affective states and motivation for nicotine and other drug use. METHODS: The present study assessed the effects of nicotine and dopamine receptor genotype on distraction by emotional pictures, during a modified spatial attention task, in 46 overnight-deprived smokers. RESULTS: Relative to placebo, 14mg nicotine patch produced shorter overall reaction times (RTs) and individuals with two dopamine type 2 receptor (DRD2) A2 alleles exhibited the greatest RT benefit from nicotine following emotionally negative pictures after the longest cue-target delay (800ms), but benefitted least from nicotine following positive pictures after the shortest delay (400ms). In contrast, at the shortest delay, A1 carriers did not benefit from nicotine following emotionally negative pictures but did following positive ones. CONCLUSIONS: These genetic differences in the effects of nicotine on attention immediately following emotionally positive versus negative stimuli may reflect differential excitatory and inhibitory transmitter processes related to approach (reward) and avoidance (punishment) sensitivities of dopamine-related neural networks that support positive and negative affect.

Nicotine differentially modulates antisaccade eye-gaze away from emotional stimuli in nonsmokers stratified by pre-task baseline performance.

RATIONALE AND OBJECTIVE: Studies indicate that nicotine enhances some aspects of attention and executive functioning and attenuates the attentional salience of emotionally negative distractors. The purpose of this study was to assess whether nicotine can enhance executive control over prepotent responses in emotional contexts in nonsmokers and whether such enhancement is greater in individuals with low baseline performance (BP). METHODS: The antisaccade task (AST) measures the inhibition of the tendency to glance in the direction of the onset of a visual stimulus and thus is an index of control over prepotent responses. Ten male and 14 female nonsmokers wore nicotine and placebo patches on counterbalanced days that included emotional picture primes and targets. RESULTS: There were significant beneficial effects of nicotine on antisaccade reaction time (RT). These beneficial effects occurred in individuals with poor and average BP, but not in high baseline performers. In slow baseline RT individuals, nicotine reduced RTs associated with negative targets in the left visual field (VF) and reduced RTs associated with positive and neutral targets in the right VF. In contrast, in the average baseline group, nicotine reduced RTs for positive targets in both VFs and neutral targets in the left VF. CONCLUSIONS: The results suggest that nicotine may produce its effects by enhancing executive functions and that the differential effects as a function of VF, target emotion, and group may also reflect lateralized differences in the effects of nicotine on brain reactivity to emotional stimuli.

Nicotine primes attention to competing affective stimuli in the context of salient alternatives.

Despite the importance of the subject, the effects of nicotine on the interplay between affect and attentional bias are not clear. This interplay was assessed with a novel design of the Primed Attentional Competition Task (PACT). It included a 200-ms duration emotional priming picture (negative, positive, or neutral) followed by a dual-target picture of two emotional faces side-by-side. A second task included an emotional priming picture followed by a single emotional target picture in a classic affective priming (CAP) task, assessing reaction time to identify the valence. Smokers completed the tasks in a double-blind repeated measures design wearing a nicotine patch on one day and a placebo patch on the other day. Consistent with hypotheses, nicotine enhanced the effectiveness of positive primes to bias first gaze-fixations (FGFs) toward neutral pictures relative to negative pictures and attenuated the effectiveness of negative primes on FGFs toward negative pictures, but did not bias performance in the CAP task where competing target stimuli were not present. These effects of nicotine on affective priming and attentional bias toward competing reinforcers may contribute to smoking motivation.