Chronic lead exposure reduces doublecortin-expressing immature neurons in young adult guinea pig cerebral cortex

Jufang Huang,Lei Shang,Xiaoxin Yan,Dan Chen,Chun-Ling Fan,Kun Xiong,Mengqi Zhang,Kai Huang,Hui Wang

doi:10.1186/1471-2202-13-82

Jufang Huang, Lei Shang + Show 7 more

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https://doi.org/10.1186/1471-2202-13-82

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Journal: BMC neuroscience	Publication Date: Jul 19, 2012
Citations: 42	License type: cc-by

Affiliation: Central South University, Shaoyang University

Abstract

BackgroundChronic lead (Pb) poisoning remains an environmental risk especially for the pediatric population, and it may affect brain development. Immature neurons expressing doublecortin (DCX+) exist around cortical layer II in various mammals, including adult guinea pigs and humans. Using young adult guinea pigs as an experimental model, the present study explored if chronic Pb exposure affects cortical DCX + immature neurons and those around the subventricular and subgranular zones (SVZ, SGZ).ResultsTwo month-old guinea pigs were treated with 0.2% lead acetate in drinking water for 2, 4 and 6 months. Blood Pb levels in these animals reached 10.27 ± 0.62, 16.25 ± 0.78 and 19.03 ± 0.86 μg/dL at the above time points, respectively, relative to ~3 μg/dL in vehicle controls. The density of DCX + neurons was significantly reduced around cortical layer II, SVZ and SGZ in Pb-treated animals surviving 4 and 6 months relative to controls. Bromodeoxyuridine (BrdU) pulse-chasing studies failed to find cellular colocalization of this DNA synthesis indicator in DCX + cells around layer II in Pb-treated and control animals. These cortical immature neurons were not found to coexist with active caspase-3 or Fluoro-Jade C labeling.ConclusionChronic Pb exposure can lead to significant reduction in the number of the immature neurons around cortical layer II and in the conventional neurogenic sites in young adult guinea pigs. No direct evidence could be identified to link the reduced cortical DCX expression with alteration in local neurogenesis or neuronal death.

Highlights

Chronic lead (Pb) poisoning remains an environmental risk especially for the pediatric population, and it may affect brain development
Elevation of blood Pb levels following chronic lead exposure Blood Pb levels were increased to 10.27 ± 0.62 μg/dL in the 2 month Pb exposure group, to 16.25 ± 0.78 μg/dL in the 4 month surviving group, and to 19.03 ± 0.86 μg/dL in the 6 month surviving group
Blood Pb levels elevated in the animal groups treated with lead acetate in a time-dependent manner at the 3 time points relative to age-matched control groups, with posthoc tests indicating no differences among the control groups (Figure 1)

Summary

Introduction

Chronic lead (Pb) poisoning remains an environmental risk especially for the pediatric population, and it may affect brain development. We and others have identified a novel group of immature neurons located around layer II of the adult cerebral cortex in relatively large mammals including guinea pigs, cats, rabbits, nonhuman primates and humans; these cells express doublecortin (DCX+) and other typical immature neuronal markers [15,16,17,18,19,20,21,22,23,24] These cortical immature neurons are more numerous in young relative to more mature animals and appear to be involved in neuronal structural plasticity [17,18,19,25]. Efforts were taken to explore if changes in cortical DCX expression overtly relate to local neurogenesis and neuronal death

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