Intact rats acquired spatial delayed alternation in a T-maze. Lesions in the anteromedial cortex or the caudate nucleus impaired retention of alternation; removal of the frontal poles did not. Delayed alternation is mediated by the cortical projection field of the mediodorsal thalamic nucleus and the caudate nucleus in a rodent species as in primates and carnivores, possibly indicating inheritance of this structure-function relation from a common ancestor. No functional resemblance between the frontal poles of rats and the prefrontal cortex of monkeys, cats, and dogs is found.

Bilateral lesions in the anteromedial neocortex or the associated part of the neostriatum abolished spontaneous alternation in rats; removal of the suprarhinal strip did not. The classical deficit of spatial choice following frontal-lobe injury is not an artifact of the learning paradigm, but can be extended to unconditioned behavior. Furthermore, the impairment is not restricted to food-reinforced or massed responses. The response-guiding role of the frontal lobe is of such wide generality in the laboratory that it can be expected to operate in the animal's usual environment as well.

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