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Molecular neurobiology of lead (Pb(2+)): effects on synaptic function Neal AP; Guilarte TRMol Neurobiol 2010[Dec]; 42 (3): 151-60Lead (Pb(2+)) is a ubiquitous environmental neurotoxicant that continues to threaten public health on a global scale. Epidemiological studies have demonstrated detrimental effects of Pb(2+) on childhood IQ at very low levels of exposure. Recently, a mechanistic understanding of how Pb(2+) affects brain development has begun to emerge. The cognitive effects of Pb(2+) exposure are believed to be mediated through its selective inhibition of the N-methyl-D: -aspartate receptor (NMDAR). Studies in animal models of developmental Pb(2+) exposure exhibit altered NMDAR subunit ontogeny and disruption of NMDAR-dependent intracellular signaling. Additional studies have reported that Pb(2+) exposure inhibits presynaptic calcium (Ca(2+)) channels and affects presynaptic neurotransmission, but a mechanistic link between presynaptic and postsynaptic effects has been missing. Recent work has suggested that the presynaptic and postsynaptic effects of Pb(2+) exposure are both due to inhibition of the NMDAR by Pb(2+), and that the presynaptic effects of Pb(2+) may be mediated by disruption of NMDAR activity-dependent signaling of brain-derived neurotrophic factor (BDNF). These findings provide the basis for the first working model to describe the effects of Pb(2+) exposure on synaptic function. Here, we review the neurotoxic effects of Pb(2+) exposure and discuss the known effects of Pb(2+) exposure in light of these recent findings.|*Neurons/cytology/drug effects/physiology[MESH]|Animals[MESH]|Behavior/drug effects[MESH]|Brain/*drug effects/physiology[MESH]|Cognition/drug effects[MESH]|Environmental Exposure[MESH]|Humans[MESH]|Intelligence/drug effects[MESH]|Lead/*toxicity[MESH]|Neuronal Plasticity/*drug effects[MESH]|Neurotoxicity Syndromes/etiology[MESH]|Receptors, N-Methyl-D-Aspartate/metabolism[MESH]|Synapses/*drug effects/*physiology[MESH] |