There is strong evidence that both acute and chronic stress can induce anxiety.
For example, in rats chronic stress and early exposure to stress by way of maternal deprivation not only induce persistent anxiety even after 21 days from the end of stress , but also induce a series of functional and morphological changes in the brain.
Particularly, stress has been linked to changes in amygdalar neural plasticity and electrophysiological responses, as well as enlargement of the amygdala (i.e., amygdalar hypertrophy).
The amygdala plays a central role in the generation and experience of fear that can give rise to anxiety
The CeA for example is known as being involved in processing explicit cue information (for example an angry face) associated with fear.
For example, the presence of unattended fearful faces is linked with increased amygdala activity.
Evidence suggests that the amygdala is involved in the generation of anxiety, with or without the presence of a threat.
Indeed, it is the central orchestrator of anxiety responses. For example, studies found that activation of the CeA and the BLA (two main components of the amygdala) is anxiogenic (i.e., cause anxiety), while their inhibition is anxiolytic (ie., reduce anxiety).
Furthermore, healthy individuals who experience anxiety show elevated amygdala activity.
Its influence on the hypothalamic-pituitary-adrenal axis (HIPA – the stress pathway) is what defines its role in anxiety. In fact, when the HIPA pathway is activated, glucocorticoids are released (stress hormones) into the bloodstream, resulting in a series of reactions designed to arouse the body into action.