Visual attraction in Drosophila larvae develops during a critical period and is modulated by crowding conditions.

The development of social behavior is poorly understood. Many animals adjust their behavior to environmental conditions based on a social context. Despite having relatively simple visual systems, Drosophila larvae are capable of identifying and are attracted to the movements of other larvae. Here, we show that Drosophila larval visual recognition is encoded by the movements of nearby larvae, experienced during a specific developmental critical period. Exposure to moving larvae, only during a specific period, is sufficient for later visual recognition of movement. Larvae exposed to wild-type body movements, during the critical period, are not attracted to the movements of tubby mutants, which have altered morphology. However, exposure to tubby, during the critical period, results in tubby recognition at the expense of wild-type recognition indicating that this is true learning. Visual recognition is not learned in excessively crowded conditions, and this is emulated by exposure, during the critical period, to food previously used by crowded larvae. We propose that Drosophila larvae have a distinct critical period, during which they assess both social and resource conditions, and that this irreversibly determines later visually guided social behavior. This model provides a platform towards understanding the regulation and development of social behavior.

Social goals in girls transitioning to adolescence: associations with psychopathology and brain network connectivity.

The motivation to socially connect with peers increases during adolescence in parallel with changes in neurodevelopment. These changes in social motivation create opportunities for experiences that can impact risk for psychopathology, but the specific motivational presentations that confer greater psychopathology risk are not fully understood. To address this issue, we used a latent profile analysis to identify the multidimensional presentations of self-reported social goals in a sample of 220 girls (9-15 years old, M = 11.81, SD = 1.81) that was enriched for internalizing symptoms, and tested the association between social goal profiles and psychopathology. Associations between social goals and brain network connectivity were also examined in a subsample of 138 youth. Preregistered analyses revealed four unique profiles of social goal presentations in these girls. Greater psychopathology was associated with heightened social goals such that higher clinical symptoms were related to a greater desire to attain social competence, avoid negative feedback and gain positive feedback from peers. The profiles endorsing these excessive social goals were characterized by denser connections among social-affective and cognitive control brain regions. These findings thus provide preliminary support for adolescent-onset changes in motivating factors supporting social engagement that may contribute to risk for psychopathology in vulnerable girls.

Individual differences in frontal alpha asymmetry moderate the relationship between acute stress responsivity and state and trait anxiety in adolescents.

Stress is a risk factor in the development and maintenance of psychopathology, particularly anxiety. Despite theory suggesting differences in stress responsivity may explain heterogeneity in anxiety, findings remain contradictory. This may be due to failure to account for individuals' neurobiological states and outdated methodologic analyses which confound conceptually and biologically distinct stress response pathways. In 145 adolescents, this study examined whether individual differences in neural activation underlying motivational states, indexed by resting frontal alpha asymmetry (FAA) before and after the Trier Social Stress Test (TSST), moderate the relationship between stress responsivity (measured by cortisol) and anxiety. Adolescents with rightward FAA activation (indexed by changes in resting FAA pre-to-post TSST) and high trait anxiety showed blunted cortisol reactivities while those with leftward FAA activation and high state anxiety showed prolonged cortisol recoveries. Our work reveals individual differences in vulnerability to psychosocial stressors and is the first study to show that FAA activation moderates the relationships between anxiety and distinct phases of the stress response in adolescents.

Triple Network Functional Connectivity During Acute Stress in Adolescents and the Influence of Polyvictimization.

BACKGROUND: Exposure to both chronic and acute stressors can disrupt functional connectivity (FC) of the default mode network (DMN), salience network (SN), and central executive network (CEN), increasing risk for negative health outcomes. During adolescence, these stress-sensitive triple networks undergo critical neuromaturation that is altered by chronic exposure to general forms of trauma or victimization. However, no work has directly examined how acute stress affects triple network FC in adolescents or whether polyvictimization-exposure to multiple categories/subtypes of victimization-influences adolescent triple network neural acute stress response. METHODS: This functional magnetic resonance imaging study examined seed-to-voxel FC of the DMN, SN, and CEN during the Montreal Imaging Stress Task. Complete data from 73 participants aged 9 to 16 years (31 female) are reported. RESULTS: During acute stress, FC was increased between DMN and CEN regions and decreased between the SN and the DMN and CEN. Greater polyvictimization was associated with reduced FC during acute stress exposure between the DMN seed and a cluster containing the left insula of the SN. CONCLUSIONS: These results indicate that acute stress exposure alters FC between the DMN, SN, and CEN in adolescents. In addition, FC changes during stress between the DMN and SN are further moderated by polyvictimization exposure.

Stress-related hippocampus activation mediates the association between polyvictimization and trait anxiety in adolescents.

Early life stress exposures are associated with adverse health outcomes and heightened anxiety symptoms in adolescents. Stress-sensitive brain regions like the hippocampus and amygdala are particularly impacted by early life adversities and are also implicated in the development of anxiety disorders. However, to date, no studies have specifically examined the neural correlates of polyvictimization (exposure to multiple categories of victimization) or the contribution of stress-sensitive neural nodes to polyvictimization's impact on mental health. To elucidate these relationships, the current study analyzed associations between polyvictimization, hippocampal and amygdalar activation during an acute stress task and trait anxiety in a sample of 80 children and adolescents aged 9-16 years (33 female participants). Results showed that polyvictimization was associated with higher trait anxiety as well as greater stress-related right hippocampus activation, and this greater hippocampal activity predicted heightened trait anxiety. Robust mediation analyses revealed that stress-related right hippocampus activation partially mediated the relationship between polyvictimization and trait anxiety. Our results expand upon the existing polyvictimization literature by suggesting a possible neurobiological pathway through which polyvictimization is connected to the etiology of mental illness.

Coordination of autonomic and endocrine stress responses to the Trier Social Stress Test in adolescence.

Dysregulations in autonomic and endocrine stress responses are linked to the emergence of psychopathology in adolescence. However, most studies fail to consider the interplay between these systems giving rise to conflicting findings and a gap in understanding adolescent stress response regulation. A multisystem framework-investigation of parasympathetic (PNS), sympathetic (SNS), and hypothalamic pituitary adrenal (HPA) axis components and their coordination-is necessary to understand individual differences in stress response coordination which contribute to stress vulnerabilities. As the first investigation to comprehensively evaluate these three systems in adolescence, the current study employed the Trier Social Stress Test in 72 typically developing adolescents (mean age = 13) to address how PNS, SNS, and HPA stress responses are coordinated in adolescence. Hypotheses tested key predictions of the Adaptive Calibration Model (ACM) of stress response coordination. PNS and SNS responses were assessed via heart rate variability (HRV) and salivary alpha amylase (sAA) respectively. HPA responses were indexed by salivary cortisol. Analyses utilized piecewise growth curve modeling to investigate these aims. Supporting the ACM theory, there was significant hierarchical coordination between the systems such that those with low HRV had higher sAA and cortisol reactivity and those with high HRV had low-to-moderate sAA and cortisol responsivity. Our novel results reveal the necessity of studying multisystem dynamics in an integrative fashion to uncover the true mechanisms of stress response and regulation during development. Additionally, our findings support the existence of characteristic stress response profiles as predicted by the ACM model.

Neural mechanisms of acute stress and trait anxiety in adolescents.

Adolescence is a critical period of heightened stress sensitivity and elevated vulnerability for developing mental illness, suggesting a possible association between stress exposure and the etiology of psychiatric disorders. In adults, aberrant neurobiological responses to acute stress relate to anxiety symptoms, yet less is known about the neural stress response in adolescents and how it relates to biological and psychological variables. Here we characterize the neurobiology of stress response in adolescents using multiple modalities, including neuroimaging, subjective stress ratings, heart rate, and cortisol data. We evaluated stress response in adolescents using the Montreal Imaging Stress Task (MIST), an acute psychosocial stressor commonly administered in adult functional magnetic resonance imaging (fMRI) studies but not previously utilized with this population. FMRI data were acquired from 101 adolescents (44 female; 9-16 years) exhibiting varied trait anxiety severity. The MIST elicited decreased high-frequency heart rate variability and increased heart rate, subjective stress and cortisol. Whole-brain analyses comparing fMRI activity during experimental versus control MIST conditions revealed stress-related activation in regions including the anterior insula, dorsal anterior cingulate cortex, and dorsolateral prefrontal cortex and deactivations in the hippocampus, ventral striatum, and putamen. Region of Interest analyses found that during acute stress (a) hippocampal deactivation corresponded to heightened cortisol release, (b) trait anxiety was associated with increased hippocampal and ventral striatum activation and decreased putamen activity, and (c) males exhibited greater putamen deactivation than females. These results provide novel evidence that the MIST is an effective stressor for adolescents. Associations between the neural acute stress response, other biological factors, and trait anxiety highlight the importance of these neurobiological mechanisms in understanding anxiety disorders.