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

BACKGROUND: 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 a...

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Autores principales: Huang, JuFang, Huang, Kai, Shang, Lei, Wang, Hui, Zhang, Mengqi, Fan, Chun-Ling, Chen, Dan, Yan, Xiaoxin, Xiong, Kun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3444321/
https://www.ncbi.nlm.nih.gov/pubmed/22812564
http://dx.doi.org/10.1186/1471-2202-13-82
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author Huang, JuFang
Huang, Kai
Shang, Lei
Wang, Hui
Zhang, Mengqi
Fan, Chun-Ling
Chen, Dan
Yan, Xiaoxin
Xiong, Kun
author_facet Huang, JuFang
Huang, Kai
Shang, Lei
Wang, Hui
Zhang, Mengqi
Fan, Chun-Ling
Chen, Dan
Yan, Xiaoxin
Xiong, Kun
author_sort Huang, JuFang
collection PubMed
description BACKGROUND: 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). RESULTS: 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. CONCLUSION: 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.
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spelling pubmed-34443212012-09-18 Chronic lead exposure reduces doublecortin-expressing immature neurons in young adult guinea pig cerebral cortex Huang, JuFang Huang, Kai Shang, Lei Wang, Hui Zhang, Mengqi Fan, Chun-Ling Chen, Dan Yan, Xiaoxin Xiong, Kun BMC Neurosci Research Article BACKGROUND: 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). RESULTS: 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. CONCLUSION: 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. BioMed Central 2012-07-19 /pmc/articles/PMC3444321/ /pubmed/22812564 http://dx.doi.org/10.1186/1471-2202-13-82 Text en Copyright ©2012 Huang et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Huang, JuFang
Huang, Kai
Shang, Lei
Wang, Hui
Zhang, Mengqi
Fan, Chun-Ling
Chen, Dan
Yan, Xiaoxin
Xiong, Kun
Chronic lead exposure reduces doublecortin-expressing immature neurons in young adult guinea pig cerebral cortex
title Chronic lead exposure reduces doublecortin-expressing immature neurons in young adult guinea pig cerebral cortex
title_full Chronic lead exposure reduces doublecortin-expressing immature neurons in young adult guinea pig cerebral cortex
title_fullStr Chronic lead exposure reduces doublecortin-expressing immature neurons in young adult guinea pig cerebral cortex
title_full_unstemmed Chronic lead exposure reduces doublecortin-expressing immature neurons in young adult guinea pig cerebral cortex
title_short Chronic lead exposure reduces doublecortin-expressing immature neurons in young adult guinea pig cerebral cortex
title_sort chronic lead exposure reduces doublecortin-expressing immature neurons in young adult guinea pig cerebral cortex
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3444321/
https://www.ncbi.nlm.nih.gov/pubmed/22812564
http://dx.doi.org/10.1186/1471-2202-13-82
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