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Behavioral inhibition and dual mechanisms of anxiety risk: Disentangling neural correlates of proactive and reactive control.

ABSTRACT: Behavioral inhibition (BI) is a temperament style characterized by heightened reactivity and negative affect in response to novel people and situations, and it predicts anxiety problems later in life. However, not all BI children develop anxiety problems, and mounting evidence suggests that how one manages their cognitive resources (cognitive control) influences anxiety risk. The present study tests whether more (proactive control) or less (reactive control) planful cognitive strategies moderate relations between early BI and later anxiety. Participants included 112 adolescents (55% female; Mage = 15.4 years) whose temperament was assessed during toddlerhood. In adolescence, participants completed an AX Continuous Performance Test while electroencephalography was recorded to disentangle neural activity related to proactive (cue-locked P3b) and reactive (probe-locked N2) control. Greater BI was associated with greater total anxiety scores only among adolescents with smaller ΔP3bs and larger ΔN2s-a pattern consistent with decreased reliance on proactive strategies and increased reliance on reactive strategies. Additionally, a larger ΔP3b was associated with greater total anxiety scores; however, this effect was largely explained by the fact that females tended to have larger ΔP3bs and greater anxiety than males. Early BI relates to risk for later anxiety specifically among adolescents who rely less on proactive strategies and more on reactive control strategies. Thus, cognitive control strategy moderates the association between developmental context (i.e., temperament) and later anxiety. The present study is the first to characterize how proactive and reactive control uniquely relate to pathways toward anxiety risk.

SUBMITTER: Valadez EA

PROVIDER: S-EPMC8477434 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:IntroductionGrowing evidence suggests that adverse experiences have long-term effects on executive functioning and underlying neural circuits. Previous work has identified functional abnormalities during inhibitory control in frontal brain regions in individuals exposed to adversities. However, these findings were mostly limited to specific adversity types such as maltreatment and prenatal substance abuse.MethodsWe used data from a longitudinal birth cohort study (n = 121, 70 females) to investigate the association between adversities and brain responses during inhibitory control. At the age of 33 years, all participants completed a stop-signal task during fMRI and an Adult Self-Report scale. We collected seven prenatal and postnatal adversity measures across development and performed a principal component analysis to capture common variations across those adversities, which resulted in a three-factor solution. Multiple regression analysis was performed to identify links between adversities and brain responses during inhibitory control using the identified adversity factors to show the common effect and single adversity measures to show the specific contribution of each adversity. To find neural correlates of current psychopathology during inhibitory control, we performed additional regression analyses using Adult Self-Report subscales.ResultsThe first adversity factor reflecting prenatal maternal smoking and postnatal psychosocial adversities was related to higher activation during inhibitory control in bilateral inferior frontal gyri, insula, anterior cingulate cortex, and middle temporal gyri. Similar results were found for the specific contribution of the adversities linked to the first adversity factor. In contrast, we did not identify any significant association between brain responses during inhibitory control and the second adversity factor reflecting prenatal maternal stress and obstetric risk or the third adversity factor reflecting lower maternal sensitivity. Higher current depressive symptoms were associated with higher activation in the bilateral insula and anterior cingulate cortex during inhibitory control.ConclusionOur findings extended previous work and showed that early adverse experiences have a long-term effect on the neural circuitry of inhibitory control in adulthood. Furthermore, the overlap between neural correlates of adversity and depressive symptomatology suggests that adverse experiences might increase vulnerability via neural alterations, which needs to be investigated by future longitudinal research.

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Behavioral inhibition and dual mechanisms of anxiety risk: Disentangling neural correlates of proactive and reactive control.

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