Fear responses promote survival, but when fear is excessive or inflexible, it becomes maladaptive. Our lab studies how the brain learns to recognize and respond to safety cues, stimuli that predict the absence of threat, and how these cues regulate fear expression through conditioned inhibition.

We focus on the ventral hippocampus (VH) and its projections to prefrontal cortex and amygdala, using in vivo fiber photometry, optogenetics, and chemogenetics to dissect circuit dynamics during safety learning. Our work has identified VH-prelimbic (PL) projections as key regulators of fear inhibition (Meyer et al., 2019, PNAS).

We are particularly interested in how the PL integrates VH input and redistributes this information to guide behavioral responding. Using dual-color photometry, we record from distinct PL neuronal populations to assess how threat, safety, and experience modulate the balance between excitation and inhibition during safety learning.

Importantly, our research extends into adolescence—a developmental window characterized by generalized and persistent fear, poor extinction learning, and high prevalence of anxiety. We are testing whether safety learning may offer a novel therapeutic avenue for adolescent populations resistant to conventional exposure-based therapies.

Balanced excitation and inhibition in the prefrontal cortex is essential for flexible and context-appropriate behavior. Our lab investigates how developing inhibitory microcircuits—particularly parvalbumin (PV+) interneurons—shape fear regulation and behavioral inhibition.

We use intersectional tagging (TRAP2) and opto/chemogenetic tools to visualize and manipulate prefrontal interneuron ensembles activated during safety learning. This allows us to determine whether these “safety engrams” are necessary or sufficient to inhibit fear, even in the absence of external safety cues.

During adolescence, PV+ interneurons undergo rapid maturation and remodeling, altering prefrontal network function. We examine how changes in interneuron structure, connectivity, and activity contribute to shifts in behavioral inhibition during development.

Adolescence is marked by heightened sensitivity to both threat and reward, and an increased prevalence of psychiatric disorders such as anxiety and depression. Many of these disorders involve dysregulated affective decision-making, especially in situations of motivational conflict.

We investigate the neural mechanisms underlying approach-avoidance conflict—when animals must weigh the opportunity for reward against the risk of threat. While adult rodents can flexibly resolve these conflicts, adolescents often exhibit excessive reward-seeking or heightened avoidance.

We combine behavioral paradigms with neural manipulation and imaging to map how developmental changes in prefrontal circuitry impact conflict resolution strategies.

This work has implications for understanding why adolescents are more likely to engage in risky behavior and may help identify circuit-level targets for improving affective regulation during this vulnerable period.

Early life experiences profoundly shape the trajectory of brain development and influence susceptibility or resilience to affective disorders later in life. Our lab investigates how positive and negative environmental inputs, such as stress exposure, learned safety, or enriched contexts, interact with neurodevelopment to impact long-term affective behavior.

We focus on how early experiences modulate prefrontal cortical circuits, including changes in neuronal activity patterns, functional connectivity, and local inhibition.

Ongoing studies use calcium imaging, immunohistochemistry, and behavioral assays to link experience-dependent circuit plasticity with longitudinal outcomes. By comparing the effects of distinct early environments on neural function and behavior, we aim to identify the mechanisms through which experience sculpts affective development—and how protective experiences might buffer against the negative consequences of early adversity.