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Indeed, given that self-righting, one of the basic mechanisms underlying resilience, has its historical roots embedded in the fields of embryology and genetics (Fishbein, 1976; Waddington, 1957), we think that it is especially unfortunate that behavioral scientists have thus far eschewed the inclusion of biological measures in their research armamentaria on resilience. In setting forth a conceptual model of biology and resilience, particular attention must be paid to the relation between the dynamic process of resilience and key components of the central nervous system, neuroendocrine, and other neurobiological systems.

Nelson (2000b) also defined neurochemical plasticity as the ability of synapses to alter their activity through aug- 11 menting the synthesis of neurotransmitters or enhancing the response of the postsynaptic receptor to the neurotransmitter. Additionally, Nelson (2000b) delineated fluctuations in cortical and subcortical metabolic activity, for example, at the site of an injury, as another possible sign of neural plasticity. In most mammalian brain regions, neuronal birth and migration take place during a discrete period of prenatal development, followed several days later by cell death (Rakic, 1988a, 1996, 1998).

Neurotrophic growth factors, embryonic forms of cell adhesion molecules, axon-guidance molecules). The presence of these molecules suggests that the degree of potential network remodeling in the mature central nervous system may be more extensive than generally thought (Lowenstein & Parent, 1999). Thus, although there is currently no unequivocal evidence that the fully developed central nervous system continues to generate new neurons and glial cells everywhere, progenitor cells with the potential to produce new cells are prevalent throughout the mature mammalian central nervous system (Gage, 2000; Lowenstein & Parent, 1999).

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