Hoff, M. P., Nadler, R. D., & Maple, T. L. (1981). Development of infant independence in a captive group of lowland gorillas. Dev Psychobiol, 14(3), 251–265.
Abstract: In March 1976, 3 lowlands gorillas (Gorilla gorilla gorilla) were born to primiparous females living with an adult male in a large compound at the field station of the Yerkes Regional Primate Research Center of Emory University. Observations of parent and infant behavior began at the birth of the infants, using several methods of data collection. This report focuses on the development of independence in these infants over the 1st 1 1/2 years of life. As expected, measures of mother-infant contact and proximity decreased with age. Several measures suggested that infant independence developed as an interactive process between mothers and infants, with primary responsibility changing over the months of study. Maternal behaviors that served to maintain mother-infant contact were found to decrease with age, with an eventual shift to infant responsibility for contact maintenance. Additionally, the adult male appeared to influence developing independence as reflected in the maternal protectiveness evoked by his behavior.
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Cowley, J. J., & Griesel, R. D. (1966). The effect on growth and behaviour of rehabilitating first and second generation low protein rats. Anim. Behav., 14(4), 506–517.
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Stamps, J. A. (2007). Growth-mortality tradeoffs and 'personality traits' in animals. Ecol Lett, 10(5), 355–363.
Abstract: Consistent individual differences in boldness, reactivity, aggressiveness, and other 'personality traits' in animals are stable within individuals but vary across individuals, for reasons which are currently obscure. Here, I suggest that consistent individual differences in growth rates encourage consistent individual differences in behavior patterns that contribute to growth-mortality tradeoffs. This hypothesis predicts that behavior patterns that increase both growth and mortality rates (e.g. foraging under predation risk, aggressive defense of feeding territories) will be positively correlated with one another across individuals, that selection for high growth rates will increase mean levels of potentially risky behavior across populations, and that within populations, faster-growing individuals will take more risks in foraging contexts than slower-growing individuals. Tentative empirical support for these predictions suggests that a growth-mortality perspective may help explain some of the consistent individual differences in behavioral traits that have been reported in fish, amphibians, reptiles, and other animals with indeterminate growth.
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Gomez, J. - C. (2005). Species comparative studies and cognitive development. Trends. Cognit. Sci., 9(3), 118–125.
Abstract: The comparative study of infant development and animal cognition brings to cognitive science the promise of insights into the nature and origins of cognitive skills. In this article, I review a recent wave of comparative studies conducted with similar methodologies and similar theoretical frameworks on how two core components of human cognition--object permanence and gaze following--develop in different species. These comparative findings call for an integration of current competing accounts of developmental change. They further suggest that evolution has produced developmental devices capable at the same time of preserving core adaptive components, and opening themselves up to further adaptive change, not only in interaction with the external environment, but also in interaction with other co-developing cognitive systems.
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Branchi, I., Bichler, Z., Berger-Sweeney, J., & Ricceri, L. (2003). Animal models of mental retardation: from gene to cognitive function. Neurosci Biobehav Rev, 27(1-2), 141–153.
Abstract: About 2-3% of all children are affected by mental retardation, and genetic conditions rank among the leading causes of mental retardation. Alterations in the information encoded by genes that regulate critical steps of brain development can disrupt the normal course of development, and have profound consequences on mental processes. Genetically modified mouse models have helped to elucidate the contribution of specific gene alterations and gene-environment interactions to the phenotype of several forms of mental retardation. Mouse models of several neurodevelopmental pathologies, such as Down and Rett syndromes and X-linked forms of mental retardation, have been developed. Because behavior is the ultimate output of brain, behavioral phenotyping of these models provides functional information that may not be detectable using molecular, cellular or histological evaluations. In particular, the study of ontogeny of behavior is recommended in mouse models of disorders having a developmental onset. Identifying the role of specific genes in neuropathologies provides a framework in which to understand key stages of human brain development, and provides a target for potential therapeutic intervention.
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