Oxford Handbook of Developmental Behavioral Neuroscience (Oxford Library of Neuroscience)
The Oxford Handbook of Developmental Behavioral Neuroscience is a seminal reference work in the burgeoning field of developmental behavioral neuroscience, which has emerged in recent years as an important sister discipline to developmental psychobiology. This handbook, part of the Oxford Library of Neuroscience, provides an introduction to recent advances in research at the intersection of developmental science and behavioral neuroscience, while emphasizing the central research perspectives of developmental psychobiology. Contributors to the Oxford Handbook of Developmental Behavioral Neuroscience are drawn from a variety of fields, including developmental psychobiology, neuroscience, comparative psychology, and evolutionary biology, demonstrating the opportunities to advance our understanding of behavioral and neural development through enhanced interactions among parallel disciplines.
In a field ripe for collaboration and integration, the Oxford Handbook of Developmental Behavioral Neuroscience provides an unprecedented overview of conceptual and methodological issues pertaining to comparative and developmental neuroscience that can serve as a roadmap for researchers and a textbook for educators. Its broad reach will spur new insights and compel new collaborations in this rapidly growing field.
a subset of cortical neurons and that this response appeared to be organized into discrete columns perpendicular to the cortical surface (Hubel & Wiesel, 1959, 1962). They termed these structures “ocular dominance columns.” In subsequent seminal experiments, Hubel and Wiesel demonstrated that monocular eye closure followed by recovery in young kittens shifts eye-speciﬁc activation of neurons in the primary visual cortex in favor of the open eye (Wiesel & Hubel, 1963, 1965a). By using monocular
Correspondences Between the Hypothetical Ancestral Genes and Those of the Hox System in Insects and Mammals Drosophila 5′ lab Pb zen Dfd Ser Antp Ubx abd-A abd-B Common ancestor (hypothetical) Mouse Chromosome 11 Chromosome 6 ← lab ← Pb → Hoxb1 → Hoxb2 Hoxb3 Hoxa1 Hoxa2 Hoxa3 ← Dfd → Hoxb4 Hoxb5 → Hoxb6 Hoxb7 Hoxb8 → Hoxb9 Hoxa4 Hoxa5 Hoxa6 Hoxa7 ← Antp ← abd-B 3′ Hoxb13 Hoxa9 Hoxa10 Hoxa11 Hoxa13 Chromosome 15 Chromosome 2 Hox1d Hoxb3 Hoxc4 Hoxc5 Hoxc6 Hoxd4 Hoxc8 Hoxc9 Hoxc10
independently selected. Rather, it seems much more likely that once the pro- and anti-PCD genetic machinery was in place, then excess cells could be deleted or retained using so-called “social” controls (Raﬀ, 1992) involving evolutionarily conserved cell–cell interactions (e.g., trophic factor signaling) that may have been selected for reasons other than the control of cell death (Amiesen, 2004; Jaaro, Beck, Conticello, & Fainzilber, 2001), but that were co-opted in the service of PCD. In
neurogenesis. Science, 225, 1258–1265. Cregan, S. P., Fortin, A., MacLaurin, J. G., Callaghan, S. M., Cecconi, F., Yu, S. W., et al. (2006). Apoptosis-inducing factor is involved in the regulation of caspase-independent neuronal cell death. Journal of Cell Biology, 158(3), 507–517. Cunningham, T. J. (1982). Naturally occurring neuron death and its regulation by developing neural pathways. International Review of Cytology, 74, 163–186. Cusato, K., Stagg, S. B., & Reese, B. E. (2001). Two phases of
basic principle of biological design is also evident in the concerted development of the various functional and structural properties of neurons and neuronal networks. At the level of cellular electrophysiology, immature neurons have a very high input resistance (small currents lead to large voltage changes), and the immature PSPs/PSCs and action potentials are slower than in the adult. In contrast to the strikingly fast changes seen at the structural level, it is as if the whole immature nervous