In the lactating rat, the neural stimulus of suckling not only acutely releases PRL but also maintains the responsiveness of PRL regulatory mechanisms to subsequent nursing stimuli. Beginning near midlactation exteroceptive pup stimuli (ECS) can acutely release PRL. We have examined the capacity of this signal also to maintain the responsiveness of PRL release mechanisms to subsequent suckling stimuli. On day 14 postpartum lactating rats were either isolated from their young or exposed to ECS (without suckling) for approximately 24 h. When both groups were later nursed, plasma PRL of mothers earlier exposed to ECS rose significantly higher than that of subjects previously isolated from their young. Suckling produced a significant depletion in pituitary PRL and GH concentrations of ECS-exposed mothers; it did not produce a similar depletion in the pituitaries of the previously isolated group. When the pups were returned for suckling, ECS-exposed mothers began to nurse their pups substantially faster than did females of the isolated group. During the 6 h after nursing, the mammary glands of ECS-exposed mothers secreted milk at twice the rate of mammary glands of the isolated females. We conclude that ECS can maintain the capacity of neuroendocrine mechanisms to respond to galactopoetic hormone-releasing stimuli (consequently enhancing milk secretion) and support the maternal behavior pattern necessary for suckling to occur. As a result, ECS may become an important factor during later stages of lactation, compensating for the decline in suckling stimuli known to occur at that time.