The exact pathophysiology of anxiety is unknown. However, it is believed that stimulation of the amygdala via sensory input leads to stimulation of the fear network. The amygdala then stimulates the locus coeruleus (increasing NE release), hypothalamus (activating HPA axis), and the gray matter (leading to a change in behaviour).
The graphic also shows the relationship serotonin has with the various components of the fear network (from projections from the Raphe nuclei).
Panic attacks, which include symptoms such as feelings of anxiety, heart palpitations, and sweating can be precipitated by increased noradrenergic neurotransmission.
Extra info: Panic attacks often arise from a small stimulus which can cause enough catecholamine release to precipitate an anxiety attack.
Hypervigilance arises from noradrenergic firing from locus coeruleus.
Extra info: Hypervigilance is another symptom that results from an excess in norepinephrine.
Serotonin dysregulation in the raphe nuclei is associated with anxiety disorders.