Fig. 15.

Pre-training orbitofrontal cortical lesions do not impair delay conditioning as much as trace conditioning. Scalar β _O in the orbitofrontal cortex (Eq. 7) was progressively decreased to simulate a lesion. In (a) and (b), the unlesioned normal case = solid line, 5 % lesion = dashed line, and 10 % lesion = dotted line. The conditioned stimulus (CS) and unconditioned stimulus (US) inputs were chosen as in Fig. 14. The results of retention testing due to CS presentation are shown by graphing the activities of sensory cortex (S), orbitofrontal cortex (O), hippocampus (H), amygdala (A), hippocampal adaptive timing (R) and pontine nuclei (P): (a) Delay conditioning with five acquisition trials. (b) Trace conditioning with 20 acquisition trials. (c) Complete lesions after delay conditioning with five acquisition trials do not impact the ability to perform the conditioned response (CR) as reflected in R and P amplitudes, although timing of P is impaired. (d) Complete orbitofrontal lesions after trace conditioning with 20 acquisition trials greatly reduce the ability to perform the CR as reflected in collapsed R and P amplitudes, and a failure of P timing. Thus orbitofrontal cortex is required for performance after trace conditioning in the data and the model