Abstract
Lead (Pb) is found to impair cognitive function. Synaptic structural plasticity is considered to be the physiological basis of synaptic functional plasticity and has been recently found to play important roles in learning and memory. To study the effect of Pb on spatial learning and memory at different developmental stages, and its relationship with alterations of synaptic structural plasticity, postnatal rats were randomly divided into three groups: Control; Pre-weaning Pb (Parents were exposed to 2 mM PbCl2 3 weeks before mating until weaning of pups); Post-weaning Pb (Weaned pups were exposed to 2 mM PbCl2 for 9 weeks). The spatial learning and memory of rats was measured by Morris water maze (MWM) on PND 85–90. Rat pups in Pre-weaning Pb and Post-weaning Pb groups performed significantly worse than those in Control group (p<0.05). However, there was no significant difference in the performance of MWM between the two Pb-exposure groups. Before MWM (PND 84), the number of neurons and synapses significantly decreased in Pre-weaning Pb group, but not in Post-weaning Pb group. After MWM (PND 91), the number of synapses in Pre-weaning Pb group increased significantly, but it was still less than that of Control group (p<0.05); the number of synapses in Post-weaning Pb group was also less than that of Control group (p<0.05), although the number of synapses has no differences between Post-weaning Pb and Control groups before MWM. In both Pre-weaning Pb and Post-weaning Pb groups, synaptic structural parameters such as thickness of postsynaptic density (PSD), length of synaptic active zone and synaptic curvature increased significantly while width of synaptic cleft decreased significantly compared to Control group (p<0.05). Our data demonstrated that both early and late developmental Pb exposure impaired spatial learning and memory as well as synaptic structural plasticity in Wistar rats.
Highlights
Lead (Pb) is an abundantly existing heavy-metal pollutant in the environment and is a strong toxicant for the development of central nervous system (CNS) in children and animals [1]
Pre-weaning Pb exposure reduces the number of neurons in the hippocampi of rat pups The Nissl staining of rat hippocampus showed that there were fewer positive neurons in Pb group compared to the control group (p,0.05, Fig. 2 and Table 3)
During the early developmental stage of CNS, neurogenesis is the selfproliferation of neural progenitor cells and their differentiation into neuronal cells
Summary
Lead (Pb) is an abundantly existing heavy-metal pollutant in the environment and is a strong toxicant for the development of central nervous system (CNS) in children and animals [1]. Cognitive impairments including various aspects of learning and memory are major clinical symptoms of lead-poisoned children [2,3,4,5]. Developmental Pb exposure has been found to impair learning and memory in animals via affecting the synaptic functional plasticity, i.e. long-term potentiation (LTP) or long-term depression (LTD) [8, 9]. LTP and LTD are typical representations of synaptic functional plasticity and have been considered as physiological models of learning and memory [10, 11]. Chronic developmental low-level Pb exposure (i.e. gestation day 16 to postnatal day 114) significantly reduced the BrdU positive cellsinthe dentate granule cell (DG) layer of adult rat hippocampus at 28 days after the last injection of BrdU it was not found to impair the spatial learning, indicating that early developmental Pb exposure might affect the neurogenesis and possible other aspects of synaptic structural plasticity in rat hippocampus [15]
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