The amygdala, panic disorder, and cardiovascular responses.

The amygdala is implicated in a number of emotional responses including conditioned fear and anxiety, and it appears to regulate the behavioral and autonomic responses associated with such emotional responses. The basolateral nucleus of the amygdala (BLA) is under tonic GABAergic inhibition, and acutely blocking this inhibition results in increased anxiety-like behavior, conditioned avoidance, and sympathetically mediated cardiovascular activation. By contrast, activation of the BLA with the stress-related neuropeptide corticotropin-releasing factor results in anxiety-like behavior, but not cardiovascular activation. Furthermore, repeated activation of this region with subthreshold GABA blockade or corticotropin-releasing factor-mediated excitation (priming) results in a chronic anxiety-like state, with susceptibility to panic-like arousal following intravenous lactate infusions. The chronic anxiety state appears to result from a loss of basal inhibitory drive in the BLA as a result of NMDA-dependent synaptic plasticity involving cyclic AMP and calcium calmodulin kinase II (CAM KII)-mediated changes. The lactate-induced panic-like response appears to involve angiotensin-II mediated activation of the BLA. These results suggest that the BLA has a significant role in regulating anxiety, autonomic responses, and the development of anxiety disorders.