CONICET | Buscador de Institutos y Recursos Humanos

In mammals, maternal care has an essential role to ensure the survival and well-being of the offspring. Successful maternal care requires the expression of a large repertoire of offspring-directed behaviors to feed and protect the young. The initiation and maintenance of such a behavioral repertoire is driven by a complex neuroendocrine cascade triggered by pregnancy and is reinforced by interactions with the young. These hormonal and sensory signals are relayed to the neural circuits controlling different aspects of maternal behavior, and involve different neuromodulators, among which serotonin (5-HT) seems to play an important role [1-2]. Here we compared pup-oriented maternal and alloparental behaviors in two mouse models with constitutive 5-HT depletion, the Tph2-KO and the Pet1-KO mice, both maintained on a pure C57BL/6 genetic background. We report that the only common pup-oriented defect in Tph2-KO and Pet1-KO mice is a defective nursing in parturient animals and an altered nursing-like (crouching) behavior in virgin females, while pup retrieval defects are only present in Tph2-KO. Despite a normal mammary gland development and milk production, the defect in appropriate nursing is responsible for severe growth retardation and early lethality of pups born to hyposerotonergic dams. This nursing defect is due to acute rather constitutive 5-HT depletion, as it is reproduced by adult knockdown of Tph2 in the dorsal raphe nucleus in mothers with a prior normal maternal experience. We conclude that 5-HT innervation from the dorsal raphe is required for both the initiation and maintenance of a normal nursing behavior [3]. Our findings may be related to observations of reduced maternal/infant interactions in human depression.

enviar mensaje