Contents

I. Introduction 212

II. Long-term effects of postnatal inorganic lead exposure on adult neurobehavior 213

III. Long-term effects of postnatal inorganic lead exposure on NCAM polysialylation 214

IV. Discussion 217

V. Implications of NCAM polysialylation as a biomarker for lead-induced neurobehavioral deficits 218

Acknowledgments 220

References 221

Abstract Prospective studies in humans and experimental investigations in animals have correlated elevated perinatal blood lead levels with enduring

© 2002 by CRC Press LLC

behavioral and cognitive perturbations. Work in our laboratory has demonstrated prior postnatal lead exposure to result in an enduring impairment of molecular events associated with long-term memory consolidation.1 In these studies, the influence of prior lead exposure on the transient modulations of hippocampal neural cell adhesion molecule (NCAM) polysialylation state that occur in the 10-12 h posttraining period, a neuroplastic event associated with memory consolidation, were investigated. Direct quantification of pol-ysialylated dentate neurons revealed prior lead exposure to have no effect on their basal number but to significantly delay and blunt the transient increase observed in control animals at the 12 h posttraining time. Thus, lead exposure in the early postnatal period is suggested to result in enduring neuroplastic deficits, and to be most likely associated with the reordering of synaptic connections that occur during memory consolidation. Moreover, it is proposed that human serum expression of NCAM and the associated polysialyltransferase, or its regulator, protein kinase C 8, may serve as a reliable biomarker(s) for the detection of neurobehavioral toxicants.

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