Maternal depression is associated with difficulties in understanding and adequately responding to children’s emotional signals. Consequently, the interaction between mother and child is often disturbed. However, little is known about the neural correlates of these parenting difficulties. Motivated by increasing evidence of the amygdala’s important role in mediating maternal behavior, we investigated amygdala responses to child sad and happy faces in mothers with remitted major depression disorder (rMDD) relative to healthy controls.

We used the sensitivity subscale of the emotional availability scales and functional magnetic resonance imaging in 61 rMDD and 27 healthy mothers to examine the effect of maternal sensitivity on mothers’ amygdala responses to their children’s affective facial expressions.

For mothers with rMDD relative to controls, we observed decreased maternal sensitivity when interacting with their child. They also showed reduced amygdala responses to child affective faces that were associated with lower maternal sensitivity. Connectivity analysis revealed that this blunted amygdala response in rMDD mothers was functionally correlated with reduced activation in higher-order medial prefrontal areas.

Our results contribute toward a better understanding of the detrimental effects of lifetime depression on maternal sensitivity and associated brain responses. By targeting region-specific neural activation patterns, these results are a first step toward improving the prediction, prevention, and treatment of depression-related negative effects on mother–child interaction.

There are phenomenological similarities between social anxiety disorder (SAD) and posttraumatic stress disorder, such as a provoking aversive event, posttraumatic stress symptoms (e.g. intrusions) in response to these events and deficient (context-dependent) fear conditioning processes. This study investigated the neural correlates of context-dependent extinction recall and fear renewal in SAD, specifically in patients with intrusions in response to an etiologically relevant aversive social event.

During functional magnetic resonance imaging a two-day context-dependent fear conditioning paradigm was conducted in 54 patients with SAD and 54 healthy controls (HC). This included fear acquisition (context A) and extinction learning (context B) on one day, and extinction recall (context B) as well as fear renewal (contexts C and A) one day later. The main outcome measures were blood oxygen level-dependent responses in regions of interest and skin conductance responses.

Patients with SAD showed reduced differential conditioned amygdala activation during extinction recall in the safe extinction context and during fear renewal in the acquisition context compared to HC. Patients with clinically relevant intrusions moreover exhibited hypoactivation of the ventromedial prefrontal cortex (vmPFC) during extinction learning, extinction recall, and fear renewal in a novel context, while amygdala activation more strongly decreased during extinction learning and increased during fear renewal in the acquisition context compared with patients without intrusions.

Our study provides first evidence that intrusions in SAD are associated with similar deficits in context-dependent regulation of conditioned fear via the vmPFC as previously demonstrated in posttraumatic stress disorder.