We introduce a new reinforcement-learning model for the role of the hippocampus in classical conditioning, focusing on the differences between trace and delay conditioning. In the model, all stimuli are represented both as unindividuated wholes and as a series of temporal elements with varying delays. These two stimulus representations interact, producing different patterns of learning in trace and delay conditioning. The model proposes that hippocampal lesions eliminate long-latency temporal elements, but preserve short-latency temporal elements. For trace conditioning, with no contiguity between cue and reward, these long-latency temporal elements are necessary for learning adaptively timed responses. For delay conditioning, the continued presence of the cue supports conditioned responding, and the short-latency elements suppress responding early in the cue. In accord with the empirical data, simulated hippocampal damage impairs trace conditioning, but not delay conditioning, at medium-length intervals. With longer intervals, learning is impaired in both procedures, and, with shorter intervals, in neither. In addition, the model makes novel predictions about the response topography with extended cues or post-training lesions. These results demonstrate how temporal contiguity, as in delay conditioning, changes the timing problem faced by animals, rendering it both easier and less susceptible to disruption by hippocampal lesions.
['Elliot A. Ludvig', 'Richard S. Sutton', 'Eric Verbeek', 'Kehoe Ej']
A computational model of hippocampal function in trace conditioning