Figure 4.

Hypothesized circuits for Delay (A) and Trace (B) fear conditioning and extinction. (A) Hypothesized Delay circuit. During conditioning (black arrows), CS and UCS information converges in the amygdala and promotes storage-related plasticity. Plasticity in the central nucleus of the amygdala (CeA) potentiates connections to “output” areas (hypothalamic and brainstem regions) that support the fear response. During extinction (gray dashed arrows), plasticity occurs in the BLA and IL. In the BLA, extinction-related plasticity is hypothesized to incorporate new information about the CS learned during extinction. In the IL, plasticity is hypothesized to support increased input to the ITC layer of the amygdala, which inhibits the CeA to “switch off” the fear response. (B) Proposed Trace circuit. Here, CS and UCS information converges in distributed cortical areas (including the prelimbic and retrosplenial cortices), which undergo plastic changes and ultimately store the association. Plasticity is also required in the amygdala, as connections to the CeA are potentiated to drive the fear response. Trace extinction would require plasticity in the cortical areas involved in storage, to allow for the new information about the CS to be incorporated into the existing association. Extinction would also produce plastic changes in the IL, as with delay, to drive inhibition of the amygdala.