Chronic lead exposure reduces doublecortin-expressing immature neurons in young adult guinea pig cerebral cortex
- Equal contributors
1 Department of Anatomy and Neurobiology, Central South University School of Basic Medical Sciences, Changsha, Hunan, 410013, China
2 Department of Anatomy, Shaoyang Medical College, Shaoyang, Hunan, 422000, China
3 Grade 2006, Eight-year Medicine Doctor Program, Central South University Xiangya School of Medicine, Changsha, Hunan, 410013, China
Citation and License
BMC Neuroscience 2012, 13:82 doi:10.1186/1471-2202-13-82Published: 19 July 2012
Chronic 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).
Two 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.
Chronic 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.