A new brain region, the amygdalostriatal transition zone (ASt), is identified as a distinct hub that sustains fear-related activity, linking emotional appraisal to prolonged defensive actions.

The ASt is positioned as a critical neural bridge for sustained fear, filling a long-standing gap in fear circuitry models that have centered on the amygdala.

By connecting emotional associations to action selection, the ASt helps explain why fear responses persist beyond initial threat detection.

The study employs cellular-resolution calcium imaging, in vivo electrophysiology in freely moving mice, and optogenetic/chemogenetic manipulations to establish causality.

Co-authors include researchers such as Christopher Lee, James Howe, and Hao Li, reflecting a broad, collaborative effort.

Published in Neuron on September 14, 2026, with funding from NIH and private foundations, and collaboration among Salk Institute, UC San Diego, University of Utah, MIT, and others.

Led by Kay M. Tye at the Salk Institute, the study details funding and publication specifics.

The findings point toward targeted interventions that could modulate persistent fear states without broadly dampening acute threat processing.

The work highlights a previously underexplored brain region that could reshape our understanding of the neural circuitry underlying fear and defense behaviors.

ASt could become a target for therapies addressing fear-related disorders such as panic, phobias, PTSD, and anxiety, opening new avenues for treatment.

Therapeutic strategies might focus on ASt activity or its dopamine-receptor-bearing cells to lessen persistent fear while preserving early threat detection.

Causal experiments show that stimulating the ASt drives freezing and avoidance, while inhibiting it reduces defensive responses; dopamine-expressing neurons in the ASt are necessary for fear responses.