SOCIAL, EMOTIONAL, COGNITIVE, AND PHYSIOLOGICAL CORRELATES OF ELECTRONIC SOCIAL BEHAVIOR

There has been very little research that has studied the capacities that can be fostered to mitigate the risk for involvement in electronic bullying or victimization and almost no research examining positive electronic behavior. The primary goal of this dissertation was to use the General Aggression Model and Anxious Apprehension Model of Trauma to explore the underlying cognitive, emotional, and self-regulation processes that are related to electronic bullying, victimization, and prosocial behavior. In Study 1, we explored several potential interpretations of the General Aggression Model that would accurately describe the relationship that electronic self-conscious appraisal, cognitive reappraisal, and activational control may have with electronic bullying and victimization. In Study 2, we used the Anxious Apprehension Model of Trauma to explore rejection cognitions as the mediator of the relationships among emotionality (emotionality, shame, state emotion responses, and physiological arousal) and electronic bullying and victimization using structural equation modelling. In addition, we explored the role of rejection cognitions in mediating the relationship of moral disengagement with electronic bullying. In Study 3, we examined predictors of electronic prosocial behavior, such as bullying, victimization, time online, electronic proficiency, electronic self-conscious appraisals, emotionality, and self-regulation. All three studies supported the General Aggression Model as a framework to guide the study of electronic behavior, and suggest the importance of cognitive, emotional, and behavioral means of regulation in shaping electronic behavior. In addition, each study has implications for the development of high quality electronic bullying prevention and intervention research.

ROLE OF THE FRONTAL EYE FIELD, SUPERIOR COLLICULUS, AND BASAL GANGLIA IN FLEXIBLE SACCADE BEHAVIOR

A distributed network of cortical and subcortical brain regions mediates the control of voluntary behavior, but it is unclear how this complex system may flexibly shift between different behavioral events. This thesis describes the neurophysiological changes in several key nuclei across the brain during flexible behavior, using saccadic eye movements in rhesus macaque monkeys. We examined five nuclei critical for saccade initiation and modulation: the frontal eye field (FEF) in the cerebral cortex, the subthalamic nucleus (STN), caudate nucleus (CD), and substantia nigra pars reticulata (SNr) in the basal ganglia (BG), and the superior colliculus (SC) in the midbrain. The first study tested whether a ‘threshold’ theory of how neuronal activity cues saccade initiation is consistent with the flexible control of behavior. The theory suggests there is a fixed level of FEF and SC neuronal activation at which saccades are initiated. Our results provide strong evidence against a fixed saccade threshold in either structure during flexible behavior, and indicate that threshold variability might depend on the level of inhibitory signals applied to the FEF or SC. The next two studies investigated the BG network as a likely candidate to modulate a saccade initiation mechanism, based on strong inhibitory output signals from the BG to the FEF and SC. We investigated the STN and CD (BG input), and the SNr (BG oculomotor output) to examine changes across the BG network. This revealed robust task-contingent shifts in BG signaling (Chapter 3), which uniquely impacted saccade initiation according to behavioral condition (Chapters 3 and 4). The thesis concludes with a published short review of the mechanistic effects of BG deep brain stimulation (Chapter 5), and a general discussion including proof of concept saccade behavioral changes in an MPTP-induced Parkinsonian model (Chapter 6). The studies presented here demonstrate that the conditions for saccade initiation by the FEF and SC vary according to behavioral condition, while simultaneously, large-scale task dependent shifts occur in BG signaling consistent with the observed modulation of FEF and SC activity. Taken together, these describe a mechanistic framework by which the cortico-BG loop may contribute to the flexible control of behavior.