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.

Virgin female mice received hypothalamic (Group PROL-HYPO), neocortical (Group PROL-CORT), or subdermal (Group PROL-NECK) implants of approximately .07 mg. prolactin or hypothalamic implants of approximately .07 mg. progesterone (Group PROG-HYPO) placed in the tips of stainless-steel tubing. Group PROL-SYST received subdermal implants of approximately 1.5 mg. dry powdered prolactin. A group of unoperated mice served as controls (Group NORM). Members of groups PROL-HYPO and PROL-SYST retrieved pups significantly faster than all the other groups, spent more time in the nest licking them, and built superior nests. Group PROG-HYPO also built superior nests, but their retrieving behavior was indistinguishable from controls. The results suggest that prolactin facilitates maternal behavior, and its site of action is in the anterior hypothalamus.

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Male and female B6D2Fi hybrid mice were given septal lesions (Group SEPT), cortical lesions (CORT), or served as unoperated controls (NORM). The mice were trained for food reward in a two-lever singlealternation task. Performance of Group SEPT was significantly better than that of the control group; Groups CORT and NORM did not differ from each other. The results are incompatible with the hypothesis that septal lesions produce a simple deficit in response inhibition or sequential behavior. It was suggested that the results might be attributed to higher response rates because of septal lesion-induced enhancement of the reward value of the food.

No abstract