Childhood irritability (i.e., proneness to anger; Leibenluft, 2017), defiance (i.e., non-compliance), and callous-unemotional (CU) traits (i.e., low empathy and guilt; Waller & Hyde, 2018) are co-occurring symptoms of several childhood psychiatric disorders, particularly those within the externalizing spectrum (Kolko & Pardini, 2010; Wakschlag et al., 2018; Waschbusch et al., 2020). For example, irritability, defiance, and CU traits are commonly comorbid symptoms among children presenting for treatment with oppositional defiant disorder (ODD) or conduct disorder (CD; Kahn et al., 2013; Scheeringa et al., 2001; Stringaris et al., 2018). This comorbidity complicates treatment as children with comorbid irritability, CU traits, and/or defiance improve less following psychosocial or pharmacological treatment (Balia et al., 2018; Colins et al., 2020; Hawes et al., 2014; Kolko & Pardini, 2010). At the same time, irritability, but not CU traits or defiance, has been linked to disruptive mood dysregulation disorder (DMDD), major depressive disorder (MDD), and bipolar disorder (Beauchaine & Tackett, 2020; Stringaris et al., 2012). To date, prior research has conceptualized and studied irritability, defiance, and CU traits as distinct symptom dimensions that separately signal risk for psychiatric disorders across the lifespan, often failing to take into account their comorbidity (Rivenbark et al., 2018; Tarter et al., 1995; Wymbs et al., 2012). One approach to better characterize what is shared versus unique between irritability, defiance, and CU traits, is to leverage neuroimaging. The use of neuroimaging, including functional magnetic resonance imaging (fMRI), can provide a biological lens from which to better understand what emerges at the level of behavior and symptoms. However, no studies have examined associations between dysfunctional neural processing and the unique versus overlapping portions of irritability, defiance, and CU traits. Further, prior research have relied on categorical group-based analysis (e.g., case-control comparisons, Hartmann & Schwenck, 2020; Stringaris et al., 2018). This classification tradition is at odds with extensive evidence that psychiatric phenomena exist on a continuum (Caspi & Moffitt, 2018; Insel, 2014; Karcher et al., 2021; Michelini et al., 2019), as well as recent initiatives, such as the Research Domain Criteria (RDoC; Cuthbert, 2014) and Hierarchical Taxonomy of Psychopathology (HiTOP; Bender, 2019; Kotov et al., 2018), which conceptualize psychiatric symptoms as disorders of neural circuits that exist along dimensions. Yet, no research has modeled the dimensional comorbidity of CU traits, defiance, and irritability. Irritability, defiance, and CU traits are all thought to emerge, in part, due to difficulties in emotion processing, including perceiving, generating, and regulating emotions (Cavanagh et al., 2014; Da Fonseca et al., 2008; Hartmann & Schwenck, 2020; Stringaris et al., 2018)(Morawetz et al., 2020). Effective emotion processing is associated with many positive psychosocial outcomes, including improved general well-being (Gross & John, 2003), social competence (Alwaely et al., 2021; Chronaki, 2021; Semrud-Clikeman, 2007), and academic achievement and satisfaction (Denham et al., 2013; Ivcevic & Brackett, 2014). In contrast, emotion processing difficulties are observed across many forms of psychopathology, including irritability, defiance, and CU traits (Cavanagh et al., 2014; Da Fonseca et al., 2008; Hartmann & Schwenck, 2020; Stringaris et al., 2018). For example, CU traits have been linked to general emotion recognition impairments with particularly marked impairment for distress cues (e.g., vocal and non-vocal expressions of sadness and fear) (Dawel et al., 2012; Marsh & Blair, 2008; Moore et al., 2019). Likewise, irritability has been associated with emotion recognition deficits, particularly with regards to the recognition of happiness (Guyer et al., 2007; Rappaport et al., 2018; Rich et al., 2008), while defiance has been linked to broad emotion recognition difficulties, regardless of emotion (Aspan et al., 2013; Rehder et al., 2017; Schwenck et al., 2014). A growing body of research has also implicated disruptions in the neural activity of brain regions implicated in these emotion processing difficulties for CU traits, defiance, and irritability (Leibenluft, 2017; Umbach & Tottenham, 2021). Here, results have been inconsistent in directionality (Aggensteiner et al., 2020; Brotman et al., 2010; Jones et al., 2009; Szabó et al., 2017; Wiggins et al., 2016). For example, irritability was linked to heightened amygdala reactivity to emotional faces in one study (Thomas et al., 2013) but to reduced amygdala reactivity specifically to fearful faces in another study (Wiggins et al., 2016). In addition, CU traits have been linked to reduced amygdala reactivity to fearful faces (Cardinale et al., 2019; Jones et al., 2009; Marsh et al., 2008; Szabó et al., 2017; Viding et al., 2012), but this finding has not been consistently replicated (Deming et al., 2022). Finally, defiance has been linked to increased amygdala reactivity to fearful faces, but not happy, sad, or neutral faces (Aggensteiner et al., 2020; Noordermeer et al., 2016). Importantly, studies have demonstrated that amygdala responses to fearful faces were positively associated to symptoms of defiance only when modeled simultaneously with CU traits (Lozier et al., 2014), highlighting the importance of considering symptom comorbidity in neurodevelopmental examinations of psychopathology. Together, these findings illustrate a complex picture, which may have arisen due to studies predominantly exploring independent associations between the neural correlates of emotion processing and childhood irritability, defiance, and CU traits (Brotman et al., 2010; Hartmann & Schwenck, 2020; Sloan et al., 2017), without considering their significant comorbidity. Thus, studies are needed that evaluate how brain reactivity during emotion processing map onto general versus specific aspects of these phenotypes. Recent empirical models suggest that emotion processing is underpinned by multiple, brain regions (Morawetz et al., 2020) with prominent neurodevelopmental models implicating the roles of the limbic system (i.e., social emotional system) and prefrontal cortex (i.e., the cognitive control system) beginning in childhood (Martin & Ochsner, 2016; Pitskel et al., 2011; Pozzi et al., 2021; Wager et al., 2008). For example, the inferior occipital gyrus (IOG), fusiform gyrus, superior temporal gyrus (STG), amygdala, orbitofrontal cortex (OFC), and insula are all implicated in the processing and recognition of emotional faces (Adolphs, 2002). Similarly, a subcortical network, which includes the amygdala, fusiform gyrus, parahippocampus, periaqueductal gray (PAG), and ventromedial prefrontal cortex (VMPFC), has been implicated in emotion perception, generation, and reactivity (Morawetz et al., 2020). Finally, a recent meta-analysis identified four regions – the amygdala, fusiform gyri, posterior superior temporal sulcus (pSTS), and ventrolateral prefrontal cortex (VLPFC) – as the core neural structures implicated in implicit emotion processing (i.e., a more automatic form of emotion processing that encompasses emotion recognition; [Gyurak et al., 2011; Pozzi et al., 2021]). However, no studies have examined differential relationships between neural activation during implicating emotion processing and irritability, defiance, or CU traits. To address this knowledge gap, the current study will use data from the Adolescent Brain and Cognitive Development (ABCD) Study (Feldstein Ewing et al., 2018; Garavan et al., 2018) to investigate shared versus specific neural markers of externalizing psychopathology. Specifically, this study will examine associations between general versus specific aspects of irritability, defiance, and CU traits and neural correlates of implicit emotion processing using the Emotional N-back (EN-back task; Barch et al., 2013; Casey et al., 2018). The EN-back task has been used in prior ABCD studies as an index of implicit emotion processing (Geckeler et al., 2022; Vargas & Mittal, 2021), with reduced activation in the fusiform gyrus, insula, and STG linked to more social impairment (Geckeler et al., 2022). Importantly, the EN-back task produces two emotional contrasts, a happy versus neutral face contrast and a fearful versus neutral face contrast. The current study will utilize both contrasts. Further, we will focus on 10 regions of interest (ROIs) that have been linked to emotion processing and implicit emotion processing based on a prior meta-analysis and extant literature (Adolphs, 2002; Gyurak et al., 2011; Martin & Ochsner, 2016; Morawetz et al., 2020; Pitskel et al., 2011; Pozzi et al., 2021, 2021; Wager et al., 2008) and that are available within the tabulated ABCD baseline and second-year follow-up dataset. Of note, tabulated imaging data utilized the Desikan-Killiany atlas (Desikan et al., 2006) for cortical regions, while subcortical structure segmentations were based on FreeSurfer (automatic segmentation) subcortical parcellations (Fischl et al., 2002). Given these considerations, a priori ROIs include: frontal pole, dorsolateral prefrontal cortex (dlPFC, made up of the caudal and rostral middle PFC), orbitofrontal cortex (OFC, made up of the lateral and medial OFC), anterior cingulate cortex (ACC, made up of the caudal and rostral ACC), superior temporal gyrus (STG), fusiform gyrus, amygdala, parahippocampal gyrus, nucleus accumbens, and insula. To determine shared versus specific factors of irritability, defiance, and CU traits in early adolescence, we will use a dimensional bifactor structural model that parses these three phenotypes into general (“shared”) and unique (“specific”) factors. While planned analyses are exploratory, we expect to find relationships between activation across the 10 ROIs outlined above (e.g., regions that have been previously implicated in emotion processing) and psychopathology. Specifically, we predict that disruptions in neural activity during the fearful versus neutral face contrast (but not the happy versus neutral face contrast) will be associated with general externalizing psychopathology. Additionally, we predict that lower reactivity within the amygdala to both fearful and happy faces will be specifically related to CU traits given extent literature has demonstrated relationships between lower amygdala reactivity and CU traits during emotion processing (Cardinale et al., 2019; Jones et al., 2009; Marsh et al., 2008; Szabó et al., 2017; Viding et al., 2012). In contrast, we predict that irritability and defiance will be related to increased activation in the amygdala for fearful versus neutral faces, but not for happy versus neural faces. As tests of robustness, we expect to replicate these findings using neuroimaging data from the second-year follow-up assessment and show that neural activation during implicit emotion processing at baseline is prospectively related to CU traits, irritability, and defiance at the second-year follow-up. Given the availability of only two imaging time points we are not adequality powered to detect developmental changes and thus no hypotheses are made regarding developmental change. It is hoped that the findings of the current study will help advance knowledge on childhood externalizing disorders and inform better diagnosis and precision treatments through the identification of specific and transdiagnostic neural markers of irritability, defiance, and CU traits.