Loss of hypothalamic corticotropin-releasing hormone markedly reduces anxiety behaviors in mice. Hypothalamic CRH neurons orchestrate complex behaviours after stress. Active avoidance: neural mechanisms and attenuation of Pavlovian conditioned responding.

Behavioral control blunts reactions to contemporaneous and future adverse events: medial prefrontal cortex plasticity and a corticostriatal network. Stressor controllability and learned helplessness: the roles of the dorsal raphe nucleus, serotonin, and corticotropin-releasing factor. Stressor controllability modulates fear extinction in humans. Perceived controllability and the development of posttraumatic stress disorder (PTSD) in crime victims. These observations indicate that CRH PVN neurons encode stress controllability and contribute to shifts between active and passive innate defensive strategies.

By contrast, stress with no outcome control prevents the emergence of this anticipatory activity and decreases subsequent escape behavior. Specifically, experimental stress with high outcome control increases CRH PVN neuron anticipatory activity, which increases escape behavior in an unrelated context. This anticipatory increase is sensitive to stressful stimuli that have high or low levels of outcome control. By assessing innate defensive behavior in a looming-shadow task, we show that the initiation of an escape response is preceded by an increase in the activity of corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus (PVN) of the hypothalamus (CRH PVN neurons). These consequences are apparent even in situations that are distinct from the stress context, but how the brain links prior stressful experience to subsequent behaviors remains poorly understood. In humans and rodents, the perception of control during stressful events has lasting behavioral consequences.

Shuttlebox on any-maze