Childhood maltreatment (CM), particularly emotional abuse (EA) and emotional neglect (EN), is a significant risk factor for the development of excessive anxiety in adulthood. However, the neurobiological mechanisms which underlie the relationship between CM and later development of anxiety are poorly understood. The purpose of this investigation is to delineate brain structure/function in adulthood which underlies the relationship between childhood EA/EN and adult anxiety. One-hundred eighty-two (n=182) adults with normal to clinical levels of anxiety underwent functional magnetic resonance imaging (fMRI) while completing a facial emotion processing task. CM history was assessed using the EA and EN subscale scores from the Childhood Trauma Questionnaire (CTQ). Anxiety symptoms were assessed using the anxiety subscale of the Brief Symptom Inventory. Gray matter volumes and functional activation and connectivity during emotion-processing trials targeted towards angry vs. happy and fearful vs. happy faces were examined. Mediation analyses were used to identify brain function/structure accounting for the relationship between self-reported childhood emotional abuse/neglect and anxiety symptoms in adulthood. Increasing activation in the insula and amygdala mediated the relationship between childhood EA/EN and anxiety, respectively. Decreasing activation and smaller gray matter volumes in the right dorsolateral prefrontal cortex mediated the relationship between childhood EN and anxiety. Decreasing connectivity between anterior insula and dorsal prefrontal seed regions with posterior medial (posterior cingulate/precuneus) and sensory/motor (precentral/postcentral gyri) cortices mediated the relationship between childhood EA/EN and anxiety symptoms. All functional effects were significant after controlling for symptoms of depression and gray matter volumes. A structural/functional interaction effect was found in the left amygdala such that the mediation effect of left amygdala activation on the relationship between EN and anxiety symptoms was strongest for those with the smallest gray matter volumes. This study provides initial evidence for a neuroetiological mechanism linking childhood emotional maltreatment to anxiety in adulthood through a potentiation of limbic and an attenuation of prefrontal responses to socioemotional threat cues. Findings from this investigation could be used in the initial construction of hypothesized neurodevelopmental models which relate early distal risk factors to endogenous brain changes that serve to predispose individuals to developing anxiety disorders as adults.