Neural systems involved in fear and anxiety measured with fear-potentiated startle

Michael Davis
2006 American Psychologist  
temic administration or intra-amygdala infusions of D-cycloserine as assessed with fear-potentiated startle in rats. A good deal is now known about the neural circuitry involved in how conditioned fear can augment a simple reflex (fear-potentiated startle). This involves visual or auditory as well as shock pathways that project via the thalamus and perirhinal or insular cortex to the basolateral amygdala (BLA). The BLA projects to the central (CeA) and medial (MeA) nuclei of the amygdala, which
more » ... project indirectly to a particular part of the acoustic startle pathway in the brainstem. N-methyl-D-aspartate (NMDA) receptors, as well as various intracellular cascades in the amygdala, are critical for fear learning, which is then mediated by glutamate acting in the CeA. Less predictable stimuli, such as a long-duration bright light or a fearful context, activate the BLA, which projects to the bed nucleus of the stria terminalis (BNST), which projects to the startle pathway much as the CeA does. The anxiogenic peptide corticotropin-releasing hormone increases startle by acting directly in the BNST. CeAmediated behaviors may represent stimulus-specific fear, whereas BNST-mediated behaviors are more akin to anxiety. NMDA receptors are also involved in extinction of conditioned fear, and both extinction in rats and exposurebased psychotherapy in humans are facilitated by an NMDA-partial agonist called D-cycloserine.
doi:10.1037/0003-066x.61.8.741 pmid:17115806 fatcat:ebuv2cpkwvcbdo2oqrui2ptq4q