What it is
Using unbiased whole-brain activity mapping in mice, the authors looked for circuits that previous adversity remodels to heighten sensitivity to later stress. The anterior hypothalamic nucleus (AHN), a region that had received little attention in the context of stress, reacted more strongly to stress in previously stressed mice and became more strongly correlated with a threat-related brain network. Miniscope imaging showed that AHN activity scales with negative valence and that prior stress increases the proportion of valence-sensitive AHN neurons. Inhibiting AHN neurons blunted stress responses and exciting them promoted those responses, and silencing the amygdala inputs to the AHN abolished sensitized stress responses.
Why it matters
Previous adversity increases sensitivity to later stressful events, but the causal changes in brain circuitry behind this have been poorly understood. The study gives causal evidence that the AHN regulates negative valence signals from the amygdala, and it identifies an amygdala-to-AHN pathway that heightens sensitivity to stressful events.
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Filed underStress Responses and Cortisol, Memory and Neural Mechanisms, Neurotransmitter Receptor Influence on Behavior
