Maternal behavior was evaluated in normal mice and in 4 groups with brain lesions (neocortex, cingulate cortex, anterior thalamic nuclei, and septum). Mice with lesions in the septum were severely impaired in maternal behavior. Mice with other lesions were not markedly impaired. These findings contrast with earlier studies which showed that cingulate lesions in rats produced poor maternal care. The deficit derived from disturbance of sequential organization of various behavioral acts involved in pup care and not from impaired motivation. It was suggested that lesion-disturbed maternal behavior arises from impaired inhibitory functions of the septum which normally prevent intrusion of out-of-order acts into the speciestypical sequence of responses comprising maternal behavior.

Two groups of rats were trained preoperatively on either a shift or a stay problem in a T-maze. Training trials consisted of two runs, an "information run" in which a subject was forced to go down one of the two arms of the T-maze, followed immediately by a "choice run" in which the subject could choose either arm. In the shift condition, rats were rewarded with wet mash only for choosing the arm opposite the one they entered on the information run. In the stay condition, rats were rewarded for entering the arm that was entered on the information run. In both conditions, rats ultimately learned to perform with median accuracy of 100%, but the shift group reached this level of performance after fewer trials than the stay group. In a subsequent phase, the delay between information runs and choice runs was increased from 0 to 30, 60, 90, 210 and then decreased back to 0 s. Choice accuracy in both groups declined as the delay increased and returned to 100% at the 0-s delay. Half of the subjects in each condition then received either lesions of the posterodorsal septum-aimed at disconnecting the septum and hippocampus-or control surgery. Postoperative retention deficits resulted from posterodorsal septal lesions in both shift and stay conditions. There was some recovery of performance but no indication of "savings" during postoperative training. These results indicate that deficits in maze performance by rats with septo-hippocampal damage are not restricted to tasks that require alternation of spatial locations. This finding falsifies the notion that maze deficits reflect a spontaneous alternation deficit or changed "spatial strategy," but it supports the hypothesis of a working memory deficit in these animals.

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Rats were trained preoperatively on contingently reinforced alternation in a T-maze. Then different matched groups of rats received lesions in the prelimbic cortex, mediodorsal thalamus, posterodorsal septum (aimed at transecting the precommissural fornix), and control operations (no brain lesions). Following a 2-week recovery period the rats were retested in the T-maze for retention of delayed alternation. Control rats were unaffected by the control operations and the testing hiatus of the recovery period. Rats with lesions in the prelimbic cortex performed at chance levels on the first postoperative session as did rats with posterodorsal septal lesions, but both groups recovered with continued experience, i.e., they could relearn the task. Rats with lesions in mediodorsal thalamus were only slightly affected by the lesions. The results suggest that a restricted field in the medial pregenual cortex, the prelimbic area, is critically involved in T-maze alternation. However, the data also suggest that a major subcortical source of afferents to prelimbic cortex, the mediodorsal nucleus of the thalamus, is not crucial for retention of contingently reinforced T-maze delayed alternation following interference with septo-hippocampal circuitry is consistent with data previously reported.

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