Infant maltreatment is a major risk factor for the development of affective disorders (e.g., depression, anxiety). Using the Scarcity-Adversity Model (SAM) in rats, which limits nesting resources from postnatal days 8–12, we previously showed that SAM-exposed dams display violent caregiving toward their pups. In adulthood, male SAM offspring show passive stress coping and a blunted corticosterone (CORT) response to stress, while females appear more resilient, showing milder behavioral/physiological effects. Here, we investigated whether infant maltreatment alters amygdalar (Amy) molecular programs. Following behavioral testing, we analyzed the expression of genes involved in stress regulation, chromatin remodeling and neural activation. SAM males showed a trend to reduced FosB expression and significant sex-specific changes in Nr3c2, Fkbp5, and Tet2 expression. Global Amy gene coexpression networks significantly differed between groups in both sexes. At the pairwise level, Bag1 strongly coexpressed with Mecp2 and Tet1 in control (C) males—a pattern absent in SAM males. In females, a strong negative Dnmt3a–Tet2 correlation in C reversed in SAM animals. Finally, a Bag1–Fkbp4 correlation present in C dams and offspring was lost in SAM groups, suggesting dysregulation of CORT receptor chaperone mechanisms. These findings suggest that infant maltreatment disrupts the coordination of Amy gene networks, potentially impairing long-term stress regulation in a sex-specific manner.