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Psychologists consider emotion regulation a critical developmental acquisition. Yet, there has been very little research on the neural underpinnings of emotion regulation across childhood and adolescence. We selected two ERP components associated with inhibitory control-the frontal N2 and frontal P3. We recorded these components before, during, and after a negative emotion induction, and compared their amplitude, latency, and source localization over age. Fifty-eight children 5-16 years of age engaged in a simple go/no-go procedure in which points for successful performance earned a valued prize. The temporary loss of all points triggered negative emotions, as confirmed by self-report scales. Both the frontal N2 and frontal P3 decreased in amplitude and latency with age, consistent with the hypothesis of increasing cortical efficiency. Amplitudes were also greater following the emotion induction, only for adolescents for the N2 but across the age span for the frontal P3, suggesting different but overlapping profiles of emotion-related control mechanisms. No-go N2 amplitudes were greater than go N2 amplitudes following the emotion induction at all ages, suggesting a consistent effect of negative emotion on mechanisms of response inhibition. No-go P3 amplitudes were also greater than go P3 amplitudes and they decreased with age, whereas go P3 amplitudes remained low. Finally, source modeling indicated a developmental decline in central-posterior midline activity paralleled by increasing activity in frontal midline regions suggestive of the anterior cingulate cortex. Negative emotion induction corresponded with an additional right ventral prefrontal or temporal generator beginning in middle childhood.

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Behavioral inhibition (BI) is a temperament associated with heightened vigilance and fear of novelty in early childhood, and social reticence and increased risk for anxiety problems later in development. However, not all behaviorally inhibited children develop signs of anxiety. One mechanism that might contribute to the variability in developmental trajectories is the recruitment of cognitive-control resources. The current study measured N2 activation, an ERP (event-related potential) associated with cognitive control, and modeled source-space activation (LORETA; Low Resolution Brain Electromagnetic Tomography) at seven years of age while children performed a go/no-go task. Activation was estimated for the entire cortex and then exported for four regions of interest: ventromedial prefrontal cortex (VMPFC), ventrolateral prefrontal cortex (VLPFC), dorsal anterior cingulate cortex (dorsal ACC), and dorsal lateral prefrontal cortex (DLPFC). BI was measured in early childhood (ages two and three years). Anxiety problems and social reticence were measured at seven years of age to ascertain stability of temperamental style. Results revealed that BI was associated with increased performance accuracy, longer reaction times, greater (more negative) N2 activation, and higher estimated dorsal ACC and DLPFC activation. Furthermore, early BI was only associated with social reticence at age 7 at higher (more negative) levels of N2 activation or higher estimated dorsal ACC or DLPFC activation. Results are discussed in the context of overcontrolled behavior contributing to social reticence and signs of anxiety in middle childhood.

Children's behavior problems may stem from ineffective cortical mechanisms for regulating negative emotions, and the success of interventions may depend on their impact on such mechanisms. We examined neurophysiological markers associated with emotion regulation in children comorbid for externalizing and internalizing problems before and after treatment. We hypothesized that treatment success would correspond with reduced ventral prefrontal activation, and increased dorsomedial prefrontal activation, at the time point of an event-related potential (ERP) associated with inhibitory control. Twenty-seven 8- to 12-year-old children (with usable data) were tested before and after a 14-week community-based treatment program and assessed as to improvement status. Fifteen 8- to 12-year-olds from the normal population (with usable data) were tested over the same interval. All children completed an emotion-induction go/no-go task while fitted with a 128-channel electrode net at each test session. ERP amplitudes, and estimates of cortical activation in prefrontal regions of interest, were measured at the peak of the "inhibitory" N2 and compared between improvers, nonimprovers, and nonclinical children. ERP amplitudes showed no group differences. However, improvers showed an overall reduction in ventral prefrontal activation from pretreatment to posttreatment, bringing them in line with nonclinical children, whereas ventral activation remained high for nonimprovers. Both improvers and nonimprovers showed high dorsal activation relative to nonclinical children. Supplementary analyses indicated that only ventral prefrontal regions, and only within the N2 time window, showed decreased activity from pre- to posttreatment, suggesting changes in regulatory processes rather than in overall emotional arousal. These cortically mediated changes may permit a reduction in the overengaged, rigid style of emotion regulation characteristic of children with behavior problems.