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Wednesday, 7 October 2026dailybeirut.com
Health
Researchers at the Salk Institute identified a small brain cluster, ASt, that maintains alertness for seconds after initial danger signals fade.
The human brain detects danger in fractions of a second, yet the sensation of fear often lingers far longer. Scientists have now pinpointed a specific neural region responsible for preventing this feeling from dissipating until the threat is completely gone.
According to findings published in the journal Neuron, neurons within the amygdala—the area tasked with triggering fear—react to threat signals almost instantly. While the body remains on high alert for dozens of seconds following this initial reaction, the mechanism sustaining this state remained unclear until recently.
Researchers from the Salk Institute for Biological Studies discovered that the Striatum Amygdala Transition (ASt) drives this prolonged response. This small cluster of cells sits between the amygdala and the striatum, a region governing motor control. The ASt possesses a unique genetic profile, and experiments confirmed its direct influence on how organisms respond to danger.
By analyzing the genetic material of 97,434 mouse brain nuclei, including those in the ASt, scientists found this region differs significantly from its neighbors. It contains a high concentration of Drd2-positive neurons, which are sensitive to dopamine. These cells comprised approximately 71% of the ASt population, whereas Drd1a neurons made up only 26%.
Electrical activity measurements conducted on ASt cells in 15 mice revealed distinct behavioral patterns. When animals heard sounds predicting either an electric shock or a sweet reward, ASt cells responded markedly to the threat signal. Unlike the amygdala, which produced only short pulses, ASt cells remained active for 20 seconds. Activity in these cells increased more than threefold when the mice calmed down.
To verify that the ASt directly controls behavior, researchers employed optogenetics, a technique using light to activate or silence neurons. Using blue laser stimulation on 18 mice, they observed immediate freezing responses during continuous activation. Conversely, localized stimulation caused the animals to avoid the laser beam.
Activating Drd2 neurons alone replicated this effect, while stimulating Drd1a cells had no impact on behavior. Balance tests on a rotating device confirmed that the mice’s immobility was a threat response rather than a loss of motor capability. Furthermore, inhibiting Drd2 cells reduced the danger response by nearly 50%, without affecting reward responses or general movement.
Scientists acknowledge constraints in their current work, noting that only one type of threat and reward was tested. Additionally, the ASt activated in response to auditory cues rather than environments typically associated with fear in mice. This suggests the region responds specifically to sensory indicators instead of broader environmental contexts.
The team plans to investigate whether these findings apply to humans. Understanding the mechanisms behind sustained fear is critical for treating post-traumatic stress disorder and anxiety disorders, where such responses become persistent.
