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<p>Adolescents are highly sensitive to peer influence and thus at higher risk of acquiring problematic behaviors through peer interactions. However, adolescents vary in the extent to which they are influenced by their peers. Resistance to peer influence (RPI), the tendency to refuse undesired peer norms and peer pressure, is one of the crucial explanations for this variation. Prior to designing effective interventive plans to improve RPI, it is important to elucidate the pathways of how RPI develops in childhood and adolescence. Therefore, the present study leverages an adopted-at-birth design and proposes a moderated mediation model to examine whether: 1) child phenotypic impulsivity mediates the association between birth parent impulsivity and adolescent RPI; 2) child phenotypic self-esteem mediates the association between birth parent self-esteem and adolescent RPI; 3) adoptive parent responsiveness buffers the impulsivity pathway; and 4) adoptive parent responsiveness strengthens the self-esteem pathway. The sample consists of 538 family triads, with adopted child, birth parents, and adoptive parents, drawn from a sample of 561 families recruited from 45 adoption agencies in the United States. Birth parents’ impulsivity and self-esteem were measured to index heritable factors for phenotypic impulsivity and self-esteem. Adoptive parents’ responsiveness was measured via home observations. Impulsivity and self-esteem of adopted adolescent were reported by their adoptive parents, whereas RPI was assessed via self-report. Covariates included adolescent sex, age, and the openness to adoption between birth parents and adoptive parents. Results of structural equation models revealed that none of the proposed mediating or moderating pathways reached statistically significant levels. Overall, girls reported higher RPI than boys. For future studies, researchers may want to consider more accurate proxies of genetic factors for impulsivity and self-esteem, and repeated measures designs.</p>

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Global cerebral ischemia (GCI) in rats has been shown to promote exploration of anxiogenic zones of the Elevated-Plus Maze (EPM) and Open Field Test (OFT). This study investigated changes in impulsive choice and/or defensive responses as possible contributors of heightened anxiogenic exploration observed after ischemia. Impulsivity was assessed using delay discounting (DD) paradigms, while the Predator Odour Test (PO) served to assess changes in defensive responses towards a naturally aversive stimulus. Male Long Evans rats underwent 9 days of autoshaping training and 24 days of DD training prior to GCI or sham surgery (n= 9/group). Post-surgery, rats completed the OFT, EPM, and PO, followed by 6 days of DD sessions. Blood droplets served to evaluate corticosterone secretion associated with PO exposure. With impulsivity being regulated through mesocorticolimbic monoaminergic pathways, we also characterized post-ischemic changes in the expression of dopamine D2 receptors (DRD2), dopamine transporters (DAT), and ΔFosB in the basolateral amygdala (BLA), nucleus accumbens core (NAcC) and shell (NAcS), and ventromedial prefrontal cortex (vmPFC) using immunohistofluorescence. Our findings revealed no impact of GCI on delay discounting rates, while PO approach behaviours were minimally affected. Nonetheless, GCI significantly reduced DRD2 and ΔFosB-ir in the NAcS and NAcC, respectively, while DAT-ir was diminished in both NAc subregions. Collectively, our findings refine the understanding of cognitive-behavioural and biochemical responses following stroke or cardiac arrest. They support significant alterations to the dopaminergic mesocorticolimbic pathway after ischemia, which are not associated with altered impulsive choice in a DD task but may influence locomotor exploration of the OFT and EPM.

Impulsivity and sleep and circadian rhythm disturbance are two core features of bipolar disorder that are elevated antecedents to bipolar disorder onset and persist even between mood episodes; their pervasive presence in bipolar disorder suggests that they may be particularly relevant to better understanding bipolar disorder etiology, onset, and course. Given considerable research demonstrating bidirectional associations between sleep and circadian rhythm disturbance and impulsivity in healthy individuals, it is surprising that little research has examined how these core features interact to impact bipolar disorder symptomatology, onset, and course. In a sample of late adolescents and young adults (N = 150) at low or high risk for developing bipolar disorder, we employed a naturalistic experiment in the context of an ecological momentary assessment (EMA) design to examine relationships between impulsivity, sleep and circadian rhythm alterations, and mood symptoms in everyday life. Furthermore, we sought to understand how the relationships between sleep and circadian rhythm alterations and mood fluctuation, collected during the EMA study, prospectively predicted mood symptom severity and mood episode onset at a 6-month follow-up. Linear regression, logistic regression, and multi-level modeling (MLM) revealed that higher impulsivity predicted increased mood symptoms during the EMA study, and less total sleep time (measured by actigraphy) predicted increased next-day EMA-assessed mood symptoms. Interaction analyses suggested that dim light melatonin onset time, total sleep time, and sleep onset latency moderated the relationship between impulsivity and mood symptoms (both next-day and at 6-month follow-up). Results are discussed in terms of their contribution to the existing literature. Findings highlight the necessity of multi-method, nuanced examination of the dynamic relationships between impulsivity and sleep and circadian disturbance within bipolar disorder. / Psychology