Incentive-related modulation of cognitive control in healthy, anxious, and depressed adolescents: development and psychopathology related differences.

In adolescence, cognitive and affective processes mature to adult levels (Steinberg, 2004, 2005). Immaturity in these processes is believed to contribute to adolescent risk taking, intensification of emotional responses, and increased risk for onset of psychopathology (Ernst, Pine, & Hardin, 2006; Steinberg, 2005). Developmental changes have specifically been reported in cognitive control processes such as response inhibition (Luna, Garver, Urban, Lazar, & Sweeney, 2004), performance monitoring (Davies, Segalowitz, & Gavin, 2004; Ladouceur, Dahl, & Carter, 2004), and affective processes such as response to rewards (Bjork et al., 2004; Crone & van der Molen, 2004; Ernst et al., 2005; Overman et al., 2004). The onset of psychopathology in adolescence signals alterations in cognitive/affective processes. Particularly, depression and anxiety manifest affective disturbances consistent with perturbations of motivational systems. Peak onset of these pathologies during adolescence may reflect vulnerability of these systems during this transition period. Study of motivational behavior from both a development and psychopathology perspective may help to clarify the nature of psychological processes that contribute to risk-taking behaviors and mood/anxiety disorders in adolescence. Recent research has used oculomotor tasks to explore cognitive processes in both adults and adolescents (Luna & Sweeney, 2004; Ridderinkhof, van den Wildenberg, Segalowitz, & Carter, 2004). These tasks provide sensitive and specific assays of cognitive control processes, and they are particularly well suited to address cognitive neuroscience questions (Luna et al., 2004). Saccadic eye movements afford exquisite measures of response preparation and response execution, which serve as proxy measures of response inhibition and response monitoring. Traditional tasks monitor saccades of two types: prosaccades (i.e., reflexive prepotent eye movements in the direction of laterally appearing visual target stimuli) and antisaccades (i.e., voluntary eye movements in the opposite direction of laterally appearing visual target stimuli). The antisaccade is a useful cognitive neuroscience tool, because it requires inhibition of the exogenously stimulus-driven prepotent prosaccade that occurs with onset of a lateralized target stimulus, as well as the generation of an endogenously driven eye movement in the opposite direction as the target (Munoz & Everling, 2004). Latency to onset of an antisaccade following appearance of a target stimulus has been used as a metric of response inhibition (Jazbec, McClure, Hardin, Pine, & Ernst, 2005; Luna et al., 2004; Ridderinkhof et al., 2004). We recently developed a saccadic eye movement task to examine the interactions between cognitive control and reward-related processes (Jazbec et al., 2006; Jazbec et al., 2005). Findings from our previous work revealed performance differences between healthy adolescents and healthy adults (Jazbec et al., 2006), and between healthy adolescents and adolescents with anxiety and/or mood disorders (Jazbec et al., 2005). While the task required performance of both prosaccades and antisaccades, previous group differences were exhibited primarily during antisaccade performance. Specifically, healthy adults were better than healthy adolescents at inhibiting reflexive prosaccades and generating antisaccadic eye movements. Additionally, incentives facilitated antisaccade performance across all groups. Incentives had a particularly strong influence in healthy adolescents, as their performance was enhanced to adult-like levels in the context of potential incentive. These findings support the notion that adolescence is a period of high sensitivity to incentives, and they suggest that adolescent reward sensitivity modulates cognitive control processes. In addition to developmental effects, healthy adolescents showed better antisaccade performance than adolescents with an anxiety and/or mood disorder. Three main questions emerged from previous findings. First, would it be possible to enhance the sensitivity of our task design to detect incentive type (reward or punishment) and incentive magnitude differences by using different values of potential reward and punishment? Such a modification would provide dose effect functions showing group differences in sensitivity to reward or punishment separately. Second, group differences in previous incentive modulation occurred almost exclusively during antisaccades. Moreover, they emerged for measures of latency but not for overall accuracy, the most frequently used index of saccade quality. Thus, would a more simplistic task design better identify unique patterns of incentive influence on cognitive function in normative development and psychopathology? By using only antisaccades and excluding prosaccades, we would facilitate interpretation of findings, while simultaneously doubling trial numbers and increasing power to detect significant effects, particularly for saccade accuracy. This approach would avoid the additional confounding effects of rule switching (switch from prosaccades to antisaccades and vice versa) and working memory (remember categorical meaning of the cue) and provide a design more directly focused on response inhibition, and the initiation and execution of internally generated actions. Third, would we improve our ability to characterize performance by enhancing the analytical method? Our previous work identified saccades based on the time and distance separating gazes. The use of a more conventional velocity-based method of saccade identification would more accurately characterize performance than our previous method of extrapolating from gazes. The present work addresses these 3 questions. To these aims, we modified the original task design by parameterizing incentive levels and employing only antisaccades. Additionally, we employed a velocity-based saccade identification method. From previous findings, we hypothesized: 1) performance would be better for healthy adults compared to healthy adolescents, and healthy adolescents compared to adolescents with anxiety or depression; 2) performance for all participants would be enhanced by incentives; 3) however, incentives would influence performance of healthy adolescents more than that of healthy adults; 4) incentives would influence performance of anxious and depressed adolescents less than that of healthy adolescents; and 5) performance would show a parametric enhancement with increasing levels of potential incentives, but with differing dose-effect curves as a function of group membership.