Abstract

Rats with lesions of caudate nucleus, of anterior cortex, of posterior cortex, of dorsal hippocampus, of ventral hippocampus or of dorsomedial thalamic structures were trained on a two-bar alternation task and in a Hebb-Williams maze. The experiments had the following principal aims: (1) to further analyze the alternation deficit previously found to follow caudate lesions; (2) to determine whether those neural structures necessary for alternation performance in the monkey, viz., frontal granular cortex, hippocampus and caudate nucleus are also necessary for alternation in the rat and (3) to test the hypothesis that Lashley's findings of increasingly deficient maze performance with increasing size of cortical lesion might be ascribed, at least partially, to increasing encroachment on an anterior cortical region critical for alternation and a posterior cortical region critical for visually guided behavior. We found that alternation was impaired by caudate lesions, by hippocampal lesions, by anterior cortex lesions and by thalamic lesions that included the dorsomedial nucleus. By contrast, Hebb-Williams maze performance was only impaired by posterior cortex lesions, by lesions that included the lateral geniculate bodies and by large medial thalamic lesions. The alternation deficit could not be accounted for in terms of changes in activity level, motivation, memory or response perseveration. As in the monkey, integrity of the caudate nucleus, the cortical projection of the dorsomedial nucleus and the hippocampus appear necessary for normal alternation performance. Finally, the present results support Hunter's interpretation that Lashley's “mass action” results may be attributed to progressive enroachment on specific “critical” regions.

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