Developmental psychobiology
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Pain sensitivity in mice can be modulated through exposure to familiar individuals. This phenomenon is considered a form of emotional contagion, thought to be an evolutionary precursor of empathy in mammals. In particular, mother-infant interactions early in life can considerably alter empathy development. ⋯ However, these differences disappeared when mice were separated from the dam 1 week earlier than the typical weaning age. Even when mice were alone, when treated with acetic acid, early weaning decreased their pain response. These results suggested that the disruption of mother-infant bonding through early weaning impairs pain contagion and modulates sensitivity to pain.
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Selective serotonin reuptake inhibitor medication exposure during the perinatal period can have a long term impact in adult offspring on neuroplasticity and the serotonergic system, but the impact of these medications during early development is poorly understood. The aim of this study was to determine the effects of developmental exposure to the SSRI, fluoxetine, on the serotonergic system, dopaminergic system, and synaptophysin density in the prefrontal cortex and hippocampus, as well as number of immature neurons in the dentate gyrus, in juvenile rat offspring at weaning. To model aspects of maternal depression, prenatal restraint stress was used. ⋯ Main findings show that developmental fluoxetine exposure to prenatally stressed offspring decreased 5-HT and 5-HIAA levels and altered the dopaminergic system in the hippocampus. Prenatal stress, regardless of fluoxetine, increased synaptophysin density in the PFC. This work indicates that early exposure to maternal stress and SSRI medication can alter brain monoamine levels and synaptophysin density in offspring at weaning.
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The human prefrontal cortex, important for executive functions, loses gray matter throughout the adolescent period. In rats, our laboratory demonstrated that a loss of neurons between adolescence and adulthood partially underlies the loss of volume, and this loss is greater in females than males. Here, we examine whether being deprived of gonadal hormones before puberty through adulthood influences the number of neurons in the medial prefrontal cortex (mPFC). ⋯ Prepubertal ovariectomy resulted in a higher number of neurons and glia and a larger volume of white matter compared to sham control littermates. Castrated males were not different from sham males on any measure. Thus ovarian hormones secreted after puberty influence the cellular composition of the medial prefrontal cortex.
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We developed a novel animal model of early life experiences in which rat pups are trained during postnatal days (PND) 10-13 in a T-maze with maternal contact as a reward (RER group) or its denial (DER group) as a mildly aversive event. Both groups of animals learn the T-maze, albeit the RER do so more efficiently. Training results in activation of the basal ganglia in the RER and of the hippocampus and prefrontal cortex in the DER. ⋯ Furthermore, DER animals have a hypofunctioning serotonergic system and express depressive-like behavior and increased aggression. However, they have increased hippocampal glucocorticoid receptors, indicative of efficient hypothalamic-pituitary-adrenal axis function, and an adaptive pattern of stress-induced corticosterone response. The DER experience with its relatively negative emotional valence results in a complex behavioral phenotype, which cannot be considered simply as adaptive or maladaptive.
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Memory flexibility is a hallmark of the human memory system. As indexed by generalization between perceptually dissimilar objects, memory flexibility develops gradually during infancy. ⋯ When challenged with a less complex change, two puppets that differed only in one feature--color, monolingual 6-month-olds were also able to generalize. These findings demonstrate early emerging differences in memory generalization in bilingual infants, and have important implications for our understanding of how early environmental variations shape the trajectory of memory development.