Striate cortex in the rat has been shown to possess precise structural and functional characteristics, and yet behavioral studies have revealed that within this cerebral area there is a curious lack of functional specificity. It is well established that primary defects in vision are produced by removals of striate cortex and by no other cortical lesion.2 However, loss of the maze habit was shown to follow supraminimal lesions to any part of the cerebrum, including the posterior part.1 Maze performance of cortically blinded rats was extremely inefficient when compared with that of normals or with peripherally blinded rats.3,6
Recently, I reviewed the literature in support of the view that striate cortex participates in nonvisual, as well as visual, functioning.5 I concluded that the evidence, though apparently decisive for the rat, is no more than suggestive for man,4 and simply does not exist for infrahuman primates.
ORBACH J. Disturbances of the Maze Habit Following Occipital Cortex Removals in Blind Monkeys. AMA Arch NeurPsych. 1959;81(1):49–54. doi:10.1001/archneurpsyc.1959.02340130069007
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