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National Institute of Environmental Health Sciences

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Publication Detail

Title: Presynaptic mechanisms of lead neurotoxicity: effects on vesicular release, vesicle clustering and mitochondria number.

Authors: Zhang, Xiao-Lei; Guariglia, Sara R; McGlothan, Jennifer L; Stansfield, Kirstie H; Stanton, Patric K; Guilarte, Tomás R

Published In PLoS One, (2015)

Abstract: Childhood lead (Pb2+) intoxication is a global public health problem and accounts for 0.6% of the global burden of disease associated with intellectual disabilities. Despite the recognition that childhood Pb2+ intoxication contributes significantly to intellectual disabilities, there is a fundamental lack of knowledge on presynaptic mechanisms by which Pb2+ disrupts synaptic function. In this study, using a well-characterized rodent model of developmental Pb2+ neurotoxicity, we show that Pb2+ exposure markedly inhibits presynaptic vesicular release in hippocampal Schaffer collateral-CA1 synapses in young adult rats. This effect was associated with ultrastructural changes which revealed a reduction in vesicle number in the readily releasable/docked vesicle pool, disperse vesicle clusters in the resting pool, and a reduced number of presynaptic terminals with multiple mitochondria with no change in presynaptic calcium influx. These studies provide fundamental knowledge on mechanisms by which Pb2+ produces profound inhibition of presynaptic vesicular release that contribute to deficits in synaptic plasticity and intellectual development.

PubMed ID: 26011056 Exiting the NIEHS site

MeSH Terms: Animals; CA1 Region, Hippocampal/physiopathology*; CA1 Region, Hippocampal/ultrastructure; Disease Models, Animal; Female; Lead/toxicity*; Microscopy, Electron, Transmission; Mitochondria/drug effects*; Neuronal Plasticity/drug effects; Presynaptic Terminals/drug effects*; Presynaptic Terminals/physiology; Rats; Rats, Long-Evans; Synaptic Vesicles/drug effects*

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