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DEVELOPMENT AND MATURATION OF THE NERVOUS SYSTEM: NEUROBIOLOGICAL BASIS OF VULNERABILITY TO ENVIRONMENTAL CONTAMINANTS.
Citation:
Barone, S. DEVELOPMENT AND MATURATION OF THE NERVOUS SYSTEM: NEUROBIOLOGICAL BASIS OF VULNERABILITY TO ENVIRONMENTAL CONTAMINANTS. Presented at Children's Environmental Health-Risk Assessment Issues and Challenges, Oakland, CA, May 1, 2000.
Description:
The susceptibility of the developing nervous system to damage following exposure to environmental contaminants is believed to be based upon the critical nature of the organizational events that occur in both a regionally- and temporally-dependent manner. The age-related susceptibility of the nervous system is based upon the protracted time over which the nervous system develops. This temporal vulnerability spans the embryonic, fetal, infant and adolescent periods. These organizational events are determined by the rate and duration of critical developmental processes like proliferation, migration, differentiation, synatopgenesis, myelination and apoptosis. Normal development of the nervous system requires the concomitant and coordinated ontogeny of all of these processes. Previously, adverse effects of prototypical developmental neurotoxicants have been shown to be mediated by effects on these developmental processes. Perturbations of these processes during development can result in long-term persistent consequences that affect the structure and function of the nervous system, and could account for qualitative differences in age-related susceptibility of the developing nervous system as compared to the adult nervous system. The presentation will focus on describing the ontogeny of these processes and a brief comparison of ontogeny in animal models and humans during development. Examples of perturbations of these processes and their outcomes will also be used to illustrate the developmental vulnerability of the nervous system. A discussion of developmental milestones and the relevance of transient effects on developmental endpoints will be presented. In addition, discussion will include consideration of how alterations in these processes may relate to toxicity through numerous mechanisms that may affect convergence of these developmental processes on possible final common pathways leading to altered neural development such as altered neuron number, cell differentiation, and/or altered connectivity. Thus, utilization of mechanistically-based constructs that include these developmental processes may improve the detection of, and reduce uncertainty about, adverse effects following developmental exposure to environmental neurotoxicants. (This abstract does not necessarily reflect USEPA policy)