The brightness-discrimination performance. of normal and posterior decorticate rats was measured in two test situations designed to provide different spatial task characteristics. A Y-maze and an open field with otherwise matched stimulus properties provided tests with many or few spatial characteristics, respectively. In contrast to predictions from visuospatial integrative interpretations of lesion consequences, the present results indicated no attenuation of the typical operative impairment when the reduced spatial-cue tasks were employed. Furthermore, this outcome was common to both simple acquisition/retention (Experiment 1) and successive discrimination reversal (Experiment 2) versions of the tasks. Interpretations of the relative contribution of memory or visuospatial integrative deficits to the measured behavioral consequences are discussed. Among alternative views advanced to account for the brightness-discrimination losses exhibited upon removal of the rat's posterior cortex are both memorial and visuospatial interpretations. In support of the former, Meyer (1972) has suggested that a preoperatively established memory is not destroyed by a lesion, but, rather, that access to the stored information is impaired. Braun, Meyer, and Meyer (1966) and lonason, Lauber, Robbins, Meyer, and Meyer (1970) have provided empirical support for this interpretation by demonstrating that an amphetamine dose that does not affect acquisition of a brightness task in naive posterior decorticates does enhance the relearning of the task in similarly lesioned animals. Le-Vere and LeVere (1982), in agreement with Meyer, have provided a retrieval-based explanation of the typical brightness-discrimination deficit. They have suggested that injury to a part of the integrative system produces a behavioral impairment wherein the neurological control of behavior is shifted to other noninjured, but less efficient, neural systems. When the organism comes to once again utilize the injured, but still functional, neurological system, performance is restored and recovery is inferred. Apart from the neurological mechanisms, this view implies that the memory is maintained and the behavioral deficit is based on a temporary inability to retrieve the previously stored information. The authors thank D. C. Riccio and P. Kasenow for their comments on an earlier version of this manuscript. Also, the help of Y. Hines in histology and M. Ryland and C. Velazquez in behavioral testing is gratefully acknowledged.