Abstract

The fear-potentiated startle paradigm measures conditioned fear by an increase in the amplitude of the acoustic startle reflex elicited in the presence of a cue previously paired with shock. Fear-potentiated startle is blocked selectively by drugs that reduce fear in humans, making it a valid test of conditioned fear in rats. The conditioned stimulus in rats activates the central nucleus of the amygdala through a pathway involving the auditory or visual thalamus, which projects via the perirhinal cortex to the amygdala. Pain information converges with conditioned stimulus information at the amygdala via parallel pathways from the posterior intralaminal nuclei of the thalamus and the insular cortex. Certain glutamate antagonists infused into the basolateral amygdala block the acquisition, but not the expression, of fear-potentiated startle, suggesting that this may be the site of plasticity during fear acquisition. The central nucleus of the amygdala projects directly and indirectly to the acoustic startle pathway so as to modulate the startle response. Fear-potentiated startle also can be measured in humans, using the eyeblink component of the startle reflex. Thus far, there is a close correspondence between results gathered in rats and humans, and the amygdala seems to be involved in fear-potentiated startle in humans.

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