Fig. 14.

Simulations of lesions of the thalamus, with equivalent effects on sensory cortex, demonstrate that the sensory cortex is required for optimal acquisition and retention in both delay and trace conditioning. To simulate partial lesions of the sensory cortex before any training trials occur, scalar β _S in the sensory cortex (Eq. 2) was progressively decreased: normal = solid line, 25 % decrease = dashed line, and 50 % decrease = dotted line. The results of retention testing by conditioned stimulus (CS) presentation are shown for sensory cortex (S), orbitofrontal cortex (O), hippocampus (H), amygdala (A), hippocampal adaptive timing (R), and the pontine nuclei (P). Vertical dashed lines mark the time of unconditioned stimulus (US) presentation during training, but not recall, trials. Vertical solid lines mark the onset and offset of the CS during training trials. Lesions to the sensory cortex weaken learning as a function of the conditioning paradigm and the extent of the lesion, with a special focus on O and P. (a) Recall after five training trials of delay conditioning in all three cases. (b) Worse trace conditioning was seen in the lesioned cases, even after 20 training trials, than in the corresponding delay conditioning cases in (a). (c) Doubling the number of training trials during delay conditioning to ten training trials improved performance in all three cases. (d) Doubling the number of training trials during trace conditioning to 40 trials improved performance in the no-lesion case, but had a negligible effect in the two lesioned cases