Abstract
Biologically-based dose-response (BBDR) paradigms incorporate mechanistic toxicological data in the derivation of quantitative models to estimate risk. Developmental lead (Pb) exposure has been long associated with deficits in intellectual ability. To date, direct estimates of toxicant-induced functional alterations in brain that may underlie cognition have been lacking, obviating the utilization of quantitative modeling for toxicological endpoints of higher brain function. The utility of the long-term potentiation (LTP) model of synaptic plasticity in the context of Pb-induced cognitive deficits is explored in the present paper. In reviewing physiological and biochemical requirements of LTP that may overlap with cellular mechanisms of Pb toxicity, a neurobiological schema is constructed upon which we can begin to explore the possibility of applying BBDR models in neurotoxicology.
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