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Lesions of the medial prefrontal cortex strongly impaired rats delayed alternation behaviour in a T-maze, both when the lesion was inflicted after the initial acquisition of the task and when the lesion was added after criterion performance had been reattained following an of the parietal cortex. Lesions of the parietal cortex did not impair this behaviour, either when the parietal lesion was inflicted after the initial acquisition of the task or when it was added to a prefrontal lesion after criterion performance had beed reattained. Combined, one stage, parietal and prefrontal lesions did not have a stronger effect on delayed alternation than did prefrontal lesions alone. These results indicate that in spite of the strong anatomical connectivity between the prefrontal and parietal "association" cortex the latter is not necessary for the recovery of delayed alternation after prefrontal lesions. In comparison with the parietal cortex, the prefrontal cortex seems to be uniquely involved in mediation of delayed alternation.
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