Differences in Discounting Behavior and Brain Responses for Food and Money Reward.

Most neuroeconomic research seeks to understand how value influences decision-making. The influence of reward type is less well understood. We used functional magnetic resonance imaging (fMRI) to investigate delay discounting of primary (i.e., food) and secondary rewards (i.e., money) in 28 healthy, normal-weighted participants (mean age = 26.77; 18 females). To decipher differences in discounting behavior between reward types, we compared how well-different option-based statistical models (exponential, hyperbolic discounting) and attribute-wise heuristic choice models (intertemporal choice heuristic, dual reasoning and implicit framework theory, trade-off model) captured the reward-specific discounting behavior. Contrary to our hypothesis of different strategies for different rewards, we observed comparable discounting behavior for money and food (i.e., exponential discounting). Higher k values for food discounting suggest that individuals decide more impulsive if confronted with food. The fMRI revealed that money discounting was associated with enhanced activity in the right dorsolateral prefrontal cortex, involved in executive control; the right dorsal striatum, associated with reward processing; and the left hippocampus, involved in memory encoding/retrieval. Food discounting, instead, was associated with higher activity in the left temporoparietal junction suggesting social reinforcement of food decisions. Although our findings do not confirm our hypothesis of different discounting strategies for different reward types, they are in line with the notion that reward types have a significant influence on impulsivity with primary rewards leading to more impulsive choices.

Choice impulsivity after repeated social stress is associated with increased perineuronal nets in the medial prefrontal cortex.

Repeated stress can predispose to substance abuse. However, behavioral and neurobiological adaptations that link stress to substance abuse remain unclear. This study investigates whether intermittent social defeat (ISD), a stress protocol that promotes drug-seeking behavior, alters intertemporal decision-making and cortical inhibitory function in the medial prefrontal cortex (mPFC). Male long evans rats were trained in a delay discounting task (DDT) where rats make a choice between a fast (1 s) small reward (1 sugar pellet) and a large reward (3 sugar pellets) that comes with a time delay (10 s or 20 s). A decreased preference for delayed rewards was used as an index of choice impulsivity. Rats were exposed to ISD and tested in the DDT 24 h after each stress episode, and one- and two-weeks after the last stress episode. Immunohistochemistry was performed in rat's brains to evaluate perineuronal nets (PNNs) and parvalbumin GABA interneurons (PV) labeling as markers of inhibitory function in mPFC. ISD significantly decreased the preference for delayed large rewards in low impulsive, but not high impulsive, animals. ISD also increased the density of PNNs in the mPFC. These results suggest that increased choice impulsivity and cortical inhibition predispose animals to seek out rewards after stress.

Associations between antipsychotics-induced weight gain and brain networks of impulsivity.

Given the unpredictable rapid onset and ubiquitous consequences of weight gain induced by antipsychotics, there is a pressing need to get insights into the underlying processes at the brain system level that will allow stratification of "at risk" patients. The pathophysiological hypothesis at hand is focused on brain networks governing impulsivity that are modulated by neuro-inflammatory processes. To this aim, we investigated brain anatomy and functional connectivity in patients with early psychosis (median age: 23 years, IQR = 21-27) using anthropometric data and magnetic resonance imaging acquired one month to one year after initiation of AP medication. Our analyses included 19 patients with high and rapid weight gain (i.e., ≥5% from baseline weight after one month) and 23 patients with low weight gain (i.e., <5% from baseline weight after one month). We replicated our analyses in young (26 years, IQR = 22-33, N = 102) and middle-aged (56 years, IQR = 51-62, N = 875) healthy individuals from the general population. In early psychosis patients, higher weight gain was associated with poor impulse control score (ß = 1.35; P = 0.03). Here, the observed brain differences comprised nodes of impulsivity networks - reduced frontal lobe grey matter volume (Pcorrected = 0.007) and higher striatal volume (Pcorrected = 0.048) paralleled by disruption of fronto-striatal functional connectivity (R = -0.32; P = 0.04). Weight gain was associated with the inflammatory biomarker plasminogen activator inhibitor-1 (ß = 4.9, P = 0.002). There was no significant association between increased BMI or weight gain and brain anatomy characteristics in both cohorts of young and middle-aged healthy individuals. Our findings support the notion of weight gain in treated psychotic patients associated with poor impulse control, impulsivity-related brain networks and chronic inflammation.

Pramipexole restores behavioral inhibition in highly impulsive rats through a paradoxical modulation of frontostriatal networks.

Impulse control disorders (ICDs), a wide spectrum of maladaptive behaviors which includes pathological gambling, hypersexuality and compulsive buying, have been recently suggested to be triggered or aggravated by treatments with dopamine D2/3 receptor agonists, such as pramipexole (PPX). Despite evidence showing that impulsivity is associated with functional alterations in corticostriatal networks, the neural basis of the exacerbation of impulsivity by PPX has not been elucidated. Here we used a hotspot analysis to assess the functional recruitment of several corticostriatal structures by PPX in male rats identified as highly (HI), moderately impulsive (MI) or with low levels of impulsivity (LI) in the 5-choice serial reaction time task (5-CSRTT). PPX dramatically reduced impulsivity in HI rats. Assessment of the expression pattern of the two immediate early genes C-fos and Zif268 by in situ hybridization subsequently revealed that PPX resulted in a decrease in Zif268 mRNA levels in different striatal regions of both LI and HI rats accompanied by a high impulsivity specific reduction of Zif268 mRNA levels in prelimbic and cingulate cortices. PPX also decreased C-fos mRNA levels in all striatal regions of LI rats, but only in the dorsolateral striatum and nucleus accumbens core (NAc Core) of HI rats. Structural equation modeling further suggested that the anti-impulsive effect of PPX was mainly attributable to the specific downregulation of Zif268 mRNA in the NAc Core. Altogether, our results show that PPX restores impulse control in highly impulsive rats by modulation of limbic frontostriatal circuits.

The interplay of childhood trauma, oxytocin, and impulsivity in predicting the onset of methamphetamine use.

BACKGROUND: Childhood trauma is associated with substance use disorders, including methamphetamine use disorder (MUD). Oxytocin, involved in social bonding, stress regulation, and reward processing, may influence addiction vulnerability and impulsivity in individuals with a history of childhood trauma. OBJECTIVE: To investigate the relationships among childhood trauma, oxytocin levels, impulsivity, and the age of first methamphetamine use in individuals with MUD. PARTICIPANTS AND SETTING: The study included 298 male participants (148 individuals with MUD and 150 healthy controls) from both probation offices and psychiatric clinics. METHODS: Childhood trauma was assessed using the Childhood Trauma Questionnaire-Short Form (CTQ-SF), impulsivity with the Barratt Impulsiveness Scale-11 (BIS-11), and plasma oxytocin levels were obtained. RESULTS: Individuals with MUD exhibited higher levels of childhood trauma, impulsivity, and lower plasma oxytocin levels compared to healthy controls. Childhood trauma was associated with a younger age of first methamphetamine use, higher impulsivity, and lower oxytocin levels among individuals with MUD. Plasma oxytocin levels partially mediated the relationship between childhood trauma and both the age of first methamphetamine use and impulsivity. Serial mediation analysis demonstrated that oxytocin levels and impulsivity sequentially mediated the relationship between childhood trauma and the age of first methamphetamine use. CONCLUSIONS: The findings reveal the complex interplay among childhood trauma, oxytocin, impulsivity, and methamphetamine use, emphasizing the importance of considering these factors in prevention and intervention strategies for MUD. Future research should explore oxytocin and impulsivity-focused interventions to mitigate the effects of childhood trauma and reduce MUD development risk.

Does Emotion-Related Impulsivity Relate to Specific ADHD Symptom Dimensions, and Do the Effects Generalize Across Comorbid Internalizing and Externalizing Syndromes?

BACKGROUND: Recent work highlights the role of emotion dysregulation in the pathology of Attention-Deficit/Hyperactivity Disorder (ADHD). As such, emotion-related impulsivity (ERI), the trait-like tendency toward disinhibited thoughts (Pervasive Influence of Feelings, PIF) and actions (Feelings Trigger Action, FTA) during heightened emotional states, may be particularly relevant. We explored whether Inattention (IN) and Hyperactivity/Impulsivity (HI), two core symptom dimensions of ADHD, would relate to distinct facets of ERI, and whether externalizing and internalizing symptoms would moderate these relations. METHOD: Using structural equation modeling, we examined hypotheses among 364 adults recruited for high internalizing and externalizing symptoms. RESULTS: We identified significant paths for FTA regressed on HI and PIF regressed on IN, supporting our hypotheses about main effects. Moderating paths were not significant. CONCLUSIONS: IN and HI correlate with distinct forms of ERI, These effects appear to generalize across co-occurring internalizing and externalizing symptoms. Theoretical and clinical implications are discussed.

Cognitive and motor impulsivity in the healthy brain, and implications for eating disorders and obesity: A coordinate-based meta-analysis and systematic review.

Alterations in the impulse-control balance, and in its neural bases, have been reported in obesity and eating disorders (EDs). Neuroimaging studies suggest a role of fronto-parietal networks in impulsive behaviour, with evaluation and anticipatory processes additionally recruiting meso-limbic regions. However, whether distinct facets of cognitive and motor impulsivity involve common vs. specific neural correlates remains unclear. We addressed this issue through Activation Likelihood Estimation (ALE) meta-analyses of fMRI studies on delay discounting (DD) and go/no-go (GNG) tasks, alongside conjunction and subtraction analyses. We also performed systematic reviews of neuroimaging studies using the same tasks in individuals with obesity or EDs. ALE results showed consistent activations in the striatum, anterior/posterior cingulate cortex, medial/left superior frontal gyrus and left supramarginal gyrus for impulsive choices in DD, while GNG tasks elicited mainly right-lateralized fronto-parietal activations. Conjunction and subtraction analyses showed: i) common bilateral responses in the caudate nucleus; ii) DD-specific responses in the ventral striatum, anterior/posterior cingulate cortex, left supramarginal and medial frontal gyri; iii) GNG-specific activations in the right inferior parietal cortex. Altered fronto-lateral responses to both tasks are suggestive of dysfunctional cortico-striatal balance in obesity and EDs, but these findings are controversial due to the limited number of studies directly comparing patients and controls. Overall, we found evidence for distinctive neural correlates of the motor and cognitive facets of impulsivity: the right inferior parietal lobe underpins action inhibition, whereas fronto-striatal regions and the left supramarginal gyrus are related to impulsive decision-making. While showing that further research on clinical samples is required to better characterize the neural bases of their behavioural changes, these findings help refining neurocognitive model of impulsivity and highlight potential translational implications for EDs and obesity treatment.

Momentary impulsivity interferes with emotion regulation strategy prioritization in everyday life in remitted depression.

BACKGROUND: Selectively prioritizing some emotion regulation (ER) strategies over others has been shown to predict well-being; however, it is unclear what mechanisms underlie this process. Impulsivity, which captures both top-down control of and bottom-up reactivity to emotions, is one potential mechanism of interest. METHODS: Using multilevel mediation modeling, we investigated whether lower ER strategy prioritization (i.e., lower between-strategy variability) mediates the relationship between greater momentary impulsivity and lower ER success in 82 individuals with remitted depression or no history of a mental disorder (1558 observations). To determine the specific effect of impulsivity, we covaried for mean regulatory effort and negative affect. RESULTS: The indirect effect of impulsivity on ER success was significant at the within-person, but not between-person, level. Specifically, in moments when individuals endorsed more impulsivity than usual, they showed less ER strategy prioritization than usual, which predicted less successful ER. Individuals who, on average, reported more impulsivity indicated lower ER strategy prioritization, but no difference in ER success. CONCLUSION: ER strategy prioritization mediated the within-person relationship between greater impulsivity and lower ER success. Interventions focused on training individuals to selectively prioritize ER strategies may improve ER success, particularly when individuals are feeling more impulsive than usual.

Positive schizotypy and Motor Impulsivity correlate with response aberrations in ventral attention network during inhibitory control.

Inhibitory control (IC) aberrations are present in various psychopathologies, including schizophrenia spectrum and personality disorders, especially in association with antisocial or violent behaviour. We investigated behavioural and neural associations between IC and psychopathology-related traits of schizotypy [Oxford-Liverpool Inventory of Feelings and Experiences (O-LIFE)], psychopathy [Triarchic Psychopathy Measure (TriPM)], and impulsivity [Barratt Impulsiveness Scale (BIS-11)], using a novel Go/No-Go Task (GNG) featuring human avatars in 78 healthy adults (25 males, 53 females; mean age = 25.96 years, SD = 9.85) and whole-brain functional magnetic resonance imaging (fMRI) in a separate sample of 22 right-handed healthy individuals (7 males, 15 females; mean age = 24.13 years, SD = 5.40). Behaviourally, O-LIFE Impulsive Nonconformity (impulsive, anti-social, and eccentric behaviour) significantly predicted 16 % of variance in false alarms (FAs). O-LIFE Unusual Experiences (positive schizotypy) and BIS-11 Motor Impulsivity predicted 15 % of d prime (d') (sensitivity index) for the fastest (400 ms) GNG trials. When examined using fMRI, higher BIS-11 Motor Impulsivity uniquely, and also together with Unusual Experiences, was associated with lower activity in the left lingual gyrus during successful inhibition (correct No-Go over baseline). Additionally, higher Impulsive Nonconformity was associated with lower activity in the caudate nucleus and anterior cingulate during No-Go compared to Go stimuli reactions. Positive schizotypy, motor, and antisocial-schizotypal impulsivity correlate with some common but mostly distinct neural activation patterns during response inhibition in areas within or associated with the ventral attention network.

Accentuated Paralimbic and Reduced Mesolimbic D2/3-Impulsivity Associations in Parkinson's Disease.

Impulsivity is a behavioral trait that is elevated in many neuropsychiatric disorders. Parkinson's disease (PD) patients can exhibit a specific pattern of reward-seeking impulsive-compulsive behaviors (ICBs), as well as more subtle changes to generalized trait impulsivity. Prior studies in healthy controls (HCs) suggest that trait impulsivity is regulated by D2/3 autoreceptors in mesocorticolimbic circuits. While altered D2/3 binding is noted in ICB+ PD patients, there is limited prior assessment of the trait impulsivity-D2/3 relationship in PD, and no prior direct comparison with patterns in HCs. We examined 54 PD (36 M; 18 F) and 31 sex- and age-matched HC (21 M; 10 F) subjects using [18F]fallypride, a high-affinity D2/3 receptor ligand, to measure striatal and extrastriatal D2/3 nondisplaceable binding potential (BPND). Subcortical and cortical assessment exclusively used ROI or exploratory-voxelwise methods, respectively. All completed the Barratt Impulsiveness Scale, a measure of trait impulsivity. Subcortical ROI analyses indicated a negative relationship between trait impulsivity and D2/3 BPND in the ventral striatum and amygdala of HCs but not in PD. By contrast, voxelwise methods demonstrated a positive trait impulsivity-D2/3 BPND correlation in ventral frontal olfactocentric-paralimbic cortex of subjects with PD but not HCs. Subscale analysis also highlighted different aspects of impulsivity, with significant interactions between group and motor impulsivity in the ventral striatum, and attentional impulsivity in the amygdala and frontal paralimbic cortex. These results suggest that dopamine functioning in distinct regions of the mesocorticolimbic circuit influence aspects of impulsivity, with the relative importance of regional dopamine functions shifting in the neuropharmacological context of PD.SIGNIFICANCE STATEMENT The biological determinants of impulsivity have broad clinical relevance, from addiction to neurodegenerative disorders. Here, we address biomolecular distinctions in Parkinson's disease. This is the first study to evaluate a large cohort of Parkinson's disease patients and age-matched healthy controls with a measure of trait impulsivity and concurrent [18F]fallypride PET, a method that allows quantification of D2/3 receptors throughout the mesocorticolimbic network. We demonstrate widespread differences in the trait impulsivity-dopamine relationship, including (1) loss of subcortical relationships present in the healthy brain and (2) emergence of a new relationship in a limbic cortical area. This illustrates the loss of mechanisms of behavioral regulation present in the healthy brain while suggesting a potential compensatory response and target for future investigation.

Inflamed but not impulsive: Acute inflammatory cytokine response does not impact prepotent response inhibition.

BACKGROUND: Prior evidence has linked inflammation with impulsivity, but most of this evidence is cross-sectional. In this study, we provoked an acute inflammatory cytokine response to see whether it lowered prepotent response inhibition on three cognitive tasks. METHOD: This study features secondary analyses from a randomized crossover trial in which 171 postmenopausal breast cancer survivors (Stage I-IIIA) each received a typhoid capsular polysaccharide vaccination and a saline placebo injection in a random sequence at two separate visits at least one month apart. Participants completed the Stroop Color-Discrepant Task, the 2-back, and the Conners Continuous Performance Test (CPT) on the computer between 5 and 7 h after the injections. They had their blood drawn once before and repeatedly after the injection to measure interleukin-1 receptor antagonist and interleukin-6 responses. RESULTS: Women committed marginally fewer errors on the Stroop color-discrepant trials after the typhoid vaccine (M = 0.36, SE = 0.08), compared to placebo (M = 0.54, SE = 0.09, p = .076). Injection type did not predict 2-back accuracy (p = .80) or CPT commission errors (p = .47). Inflammatory cytokine responses were also unrelated to the outcomes of interest (ps>.16). CONCLUSION: We found no evidence that an acute inflammatory cytokine response provokes response disinhibition - an important facet of impulsivity. In fact, our only marginally non-significant result suggested that women were better able to inhibit their prepotent responses on the Stroop after receiving the typhoid vaccine, compared to placebo. Further experimental tests of the acute inflammatory cytokine response's effect on other aspects of impulsivity are warranted. LIMITATIONS: The sample was female, primarily White, highly educated cancer survivors, and recruitment was not premised on impulsive traits or diagnosis with an impulsive-related disorder. Also, there are many facets of impulsivity, and this study only measured response inhibition.

Modeling Suicidality with Multimodal Impulsivity Characterization in Participants with Mental Health Disorder.

Introduction: Suicide is one of the leading causes of death across different age groups. The persistence of suicidal ideation and the progression of suicidal ideations to action could be related to impulsivity, the tendency to act on urges with low temporal latency, and little forethought. Quantifying impulsivity could thus help suicidality estimation and risk assessments in ideation-to-action suicidality frameworks. Methods: To model suicidality with impulsivity quantification, we obtained questionnaires, behavioral tests, heart rate variability (HRV), and resting state functional magnetic resonance imaging measurements from 34 participants with mood disorders. The participants were categorized into three suicidality groups based on their Mini-International Neuropsychiatric Interview: none, low, and moderate to severe. Results: Questionnaire and HRV-based impulsivity measures were significantly different between the suicidality groups with higher subscales of impulsivity associated with higher suicidality. A multimodal system to characterize impulsivity objectively resulted in a classification accuracy of 96.77% in the three-class suicidality group prediction task. Conclusions: This study elucidates the relative sensitivity of various impulsivity measures in differentiating participants with suicidality and demonstrates suicidality prediction with high accuracy using a multimodal objective impulsivity characterization in participants with mood disorders.

"Help Me Control My Impulses!": Adolescent Impulsivity and Its Negative Individual, Family, Peer, and Community Explanatory Factors.

The literature shows that impulsivity, prevalent in adolescence, is negatively linked with a variety of psychosocial factors (e.g., positive interpersonal relationships, emotion regulation); however, there is limited research examining the relative contribution of multiple factors for this trait nor exploring how these factors influence the associations between impulsivity and risk-related outcomes. Drawing on multiple components of the unified theory of development (i.e., psychological variables, peers subsystem, community subsystem, family processes subsystem), this cross-sectional study aims to identify explanatory psychosocial variables (i.e., early memories of warmth and safeness, rational decision-making style, resilience, emotion regulation, coping, parental attachment, social group attachment, satisfaction with school and family-related variables) that are negatively related with impulsivity, in younger (13-15) and older (16-19 years) adolescents, and explore their moderating role in the associations between this trait and some risk-related outcomes (i.e., verbal aggression, anger, self-harm, other high-risk behaviors). A representative sample of 6894 adolescents (52.9% female) living in the Azores (Portugal), with ages ranging from 13 to 19 (M = 15.4), was used. Two stepwise multiple regressions, one for each age group, revealed that only emotion regulation, parental attachment, and social group attachment had a negative effect on impulsivity in both age groups; additionally, satisfaction with teachers also had this effect in younger adolescents. The first three variables weakened the positive associations between impulsivity and the risk-related outcomes. These results suggest that the psychological system and all subsystems of the social context measured play a relevant role in explaining adolescent impulsivity and that it may be reduced by promoting emotion regulation, positive parenting practices, healthier relationships with peers, and healthier relationships with teachers.

Dopamine transporter blockade during adolescence increases adult dopamine function, impulsivity, and aggression.

Sensitive developmental periods shape neural circuits and enable adaptation. However, they also engender vulnerability to factors that can perturb developmental trajectories. An understanding of sensitive period phenomena and mechanisms separate from sensory system development is still lacking, yet critical to understanding disease etiology and risk. The dopamine system is pivotal in controlling and shaping adolescent behaviors, and it undergoes heightened plasticity during that time, such that interference with dopamine signaling can have long-lasting behavioral consequences. Here we sought to gain mechanistic insight into this dopamine-sensitive period and its impact on behavior. In mice, dopamine transporter (DAT) blockade from postnatal (P) day 22 to 41 increases aggression and sensitivity to amphetamine (AMPH) behavioral stimulation in adulthood. Here, we refined this sensitive window to P32-41 and identified increased firing of dopaminergic neurons in vitro and in vivo as a neural correlate to altered adult behavior. Aggression can result from enhanced impulsivity and cognitive dysfunction, and dopamine regulates working memory and motivated behavior. Hence, we assessed these behavioral domains and found that P32-41 DAT blockade increases impulsivity but has no effect on cognition, working memory, or motivation in adulthood. Lastly, using optogenetics to drive dopamine neurons, we find that increased VTA but not SNc dopaminergic activity mimics the increase in impulsive behavior in the Go/NoGo task observed after adolescent DAT blockade. Together our data provide insight into the developmental origins of aggression and impulsivity that may ultimately improve diagnosis, prevention, and treatment strategies for related neuropsychiatric disorders.

Jumping to conclusions bias, psychosis and impulsivity in early stages of Parkinson's disease.

OBJECTIVES: The aim was to explore the correlations between Jumping to Conclusions (JtC) tendency and neuropsychiatric features in patients with early Parkinson's disease (PD). BACKGROUND: According to few reports, PD patients with impulsive-compulsive behaviors (ICBs) are prone to working memory difficulties including JtC bias. The correlation of psychotic features and JtC tendency remains still unclear. METHODS: Healthy controls and patients within 3 years of PD onset were recruited. Participants were examined for psychotic symptoms using a 10 question PD-specific psychosis severity scale. JtC was measured by a probalistic reasoning scenario (beads task). In PD group, medication use, motor and non-motor symptoms were documented. Impulsivity was evaluated using the Questionnaire for Impulsive-Compulsive Disorders in PD (QUIP). RESULTS: The prevalence of JtC bias was 9% (6/70) in healthy individuals, compared to 32% (22/68) of PD group [p = 0.001]. No association was detected between the presence of JtC tendency and PD-associated psychosis (p = 0.216). Patients with JtC had shorter duration of PD, more tremor-dominant PD subtype and higher QUIP scores, regardless of the dopaminergic therapy (p = 0.043, p = 0.015, p = 0.007, respectively). A trend towards attention and inhibition control deficit was noticed in JtC patients. CONCLUSIONS: We found a high prevalence of JtC bias in early, cognitively intact PD population and a potential link between subthreshold ICBs and poor performance on beads task. Additional studies are needed to confirm our results and elaborate on the mechanisms that correlate impulsivity with JtC tendency, which are likely to be different from those mediating psychotic features in early PD.

Brain-derived neurotrophic factor Val66Met polymorphism moderates the relationship between impulsivity, negative emotions, and binge drinking intensity in university students.

Studies on the genetic factors involved in binge drinking (BD) and its associated traits are very rare. The aim of this cross-sectional study was to investigate differences in the association between impulsivity, emotion regulation and BD in a sample of young adults according to the rs6265/Val66Met variant in the brain-derived neurotrophic factor (BDNF) gene, a well-known candidate gene in alcohol use disorders. We recruited 226 university students (112 women), aged between 18 and 25 years old, from two centers in France. The participants completed measures related to alcohol consumption, depression severity, state anxiety levels, impulsivity (UPPS-P), and difficulties in emotion regulation [Difficulty in Emotion Regulation Scale (DERS)]. The relationship between the BD score and the clinical characteristics in the BDNF genotype groups was assessed by partial correlation analyses and moderation analyses. The partial correlation analyses showed that, in the Val/Val genotype group, the BD score was positively related to UPPS-P Lack of Premeditation and Sensation Seeking scores. In the Met carriers group, the BD score was positively related to UPPS-P Positive Urgency, lack of Premeditation, lack of Perseverance and Sensation Seeking scores and to Clarity score of the DERS. Moreover, the BD score was positively associated with depression severity and state anxiety scores. The moderation analyses revealed that BDNF Val/Met genotype moderated the relationship between several clinical variables and BD. The results of the present study support the hypothesis of common and specific vulnerability factors regarding impulsivity and emotion regulation difficulties associated with BD according to this BDNF rs6265 polymorphism.

Assessing attention and impulsivity in the variable stimulus duration and variable intertrial interval rodent continuous performance test schedules using noradrenaline receptor antagonists in female C57BL/6JRj mice.

RATIONALE: Noradrenergic dysfunction is associated with disorders of impulsivity and inattention. The rodent continuous performance test (rCPT) quantifies changes in attention and impulsivity. OBJECTIVE: To use NA receptor antagonists to examine the roles of NA on attention and impulsivity behaviours measured in the rCPT variable stimulus duration (vSD) and the variable intertrial interval (vITI) schedules. METHODS: Two cohorts of 36 female C57BL/6JRj mice were examined separately in the rCPT vSD and vITI schedules. Both cohorts received antagonists of the following adrenoceptors: α1 (doxazosin, DOX: 1.0, 3.0, 10.0 mg/kg), α2 (yohimbine, YOH: 0.1, 0.3, 1.0 mg/kg), and ß1/2 (propranolol, PRO: 1.0, 3.0, 10.0 mg/kg) in consecutive balanced Latin square designs with flanking reference measurements. The antagonists were subsequently examined for effects on locomotor activity. RESULTS: DOX showed similar effects in both schedules, improving discriminability and accuracy, and reducing responding and impulsivity, and DOX also reduced locomotor activity. YOH showed prominent effects in the vSD schedule to increase responding and impulsivity, while impairing discriminability and accuracy. YOH did not affect locomotor activity. PRO increased responding and impulsivity, decreased accuracy, but did not affect discriminability or locomotor activity. CONCLUSION: Antagonism of α2 or ß1/2 adrenoceptors caused similar increases in responding and impulsivity and worsened attentional performance, while α1 adrenoceptor antagonism showed the opposite effects. Our results suggest that endogenous NA exerts bidirectional control of most behaviours in the rCPT. The parallel vSD and vITI studies showed a substantial overlap in effects, but also some differences that indicate differing sensitivity towards noradrenergic manipulations.

Mediated and moderated associations between cumulative lifetime stressor exposure, emotional dysregulation, impulsivity, and lifetime alcohol use: A cross-sectional scoping study of UK drinkers.

Stress, trait impulsivity, and emotional dysregulation are independent predictors of alcohol use and misuse, but little is known about the potential mechanisms that link these risk factors together. To address this issue, we carried out an exploratory cross-sectional study, on UK-based participants. Our preregistered, hypothesised theoretical framework was that emotional dysregulation mediates the association between cumulative lifetime stressor exposure and lifetime alcohol use. We also hypothesised that heightened impulsivity would strengthen these relations. As hypothesised, emotional dysregulation fully mediated the relation between cumulative lifetime stressor exposure and lifetime alcohol use. Several facets of impulsivity moderated these associations. For example, as levels of negative urgency increased, the associations between cumulative lifetime stressor exposure and emotional dysregulation, emotional dysregulation and lifetime alcohol use, and lifetime stress exposure and lifetime alcohol use, via emotional dysregulation, strengthened. These preliminary findings propose a theoretically framed model which integrates several prominent risk-factors for alcohol misuse, extending prior research and generating interesting and novel lines of enquiry for longitudinal and cross-cultural analyses. The findings also highlight the potential clinical utility of screening for lifetime stress exposure while tailoring personalised treatment interventions.