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Tytuł:
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Early postnatal manganese exposure causes arousal dysregulation and lasting hypofunctioning of the prefrontal cortex catecholaminergic systems.
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Autorzy:
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Conley TE; Department of Microbiology and Environmental Toxicology, University of California, Santa Cruz, CA, USA.
Beaudin SA; Department of Microbiology and Environmental Toxicology, University of California, Santa Cruz, CA, USA.
Lasley SM; Department of Cancer Biology and Pharmacology, University of Illinois College of Medicine, Peoria, IL, USA.
Fornal CA; Department of Cancer Biology and Pharmacology, University of Illinois College of Medicine, Peoria, IL, USA.
Hartman J; Department of Microbiology and Environmental Toxicology, University of California, Santa Cruz, CA, USA.
Uribe W; Department of Microbiology and Environmental Toxicology, University of California, Santa Cruz, CA, USA.
Khan T; Department of Microbiology and Environmental Toxicology, University of California, Santa Cruz, CA, USA.
Strupp BJ; Division of Nutritional Sciences and Department of Psychology, Cornell University, Ithaca, NY, USA.
Smith DR; Department of Microbiology and Environmental Toxicology, University of California, Santa Cruz, CA, USA.
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Źródło:
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Journal of neurochemistry [J Neurochem] 2020 Jun; Vol. 153 (5), pp. 631-649. Date of Electronic Publication: 2020 Jan 10.
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Typ publikacji:
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Journal Article; Research Support, N.I.H., Extramural
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Język:
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English
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Imprint Name(s):
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Publication: 2001- : Oxford, UK : Wiley on behalf of the International Society for Neurochemistry
Original Publication: New York : Raven Press
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MeSH Terms:
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Arousal/*physiology
Dopamine Plasma Membrane Transport Proteins/*metabolism
Glial Fibrillary Acidic Protein/*metabolism
Manganese/*toxicity
Norepinephrine Plasma Membrane Transport Proteins/*metabolism
Prefrontal Cortex/*metabolism
Age Factors ; Animals ; Animals, Newborn ; Arousal/drug effects ; Male ; Manganese/administration & dosage ; Prefrontal Cortex/drug effects ; Rats ; Rats, Long-Evans
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Grant Information:
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R01 ES018990 United States ES NIEHS NIH HHS; R01 ES028369 United States ES NIEHS NIH HHS; R01ES028369 United States ES NIEHS NIH HHS; R01ES018990 United States ES NIEHS NIH HHS
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Contributed Indexing:
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Keywords: developmental exposure; dopamine; manganese; neuroinflammation; norepinephrine; prefrontal cortex
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Substance Nomenclature:
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0 (Dopamine Plasma Membrane Transport Proteins)
0 (GFAP protein, rat)
0 (Glial Fibrillary Acidic Protein)
0 (Norepinephrine Plasma Membrane Transport Proteins)
42Z2K6ZL8P (Manganese)
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Entry Date(s):
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Date Created: 20191208 Date Completed: 20201104 Latest Revision: 20240328
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Update Code:
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20240329
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PubMed Central ID:
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PMC7261255
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DOI:
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10.1111/jnc.14934
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PMID:
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31811785
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Studies have reported associations between environmental manganese (Mn) exposure and impaired cognition, attention, impulse control, and fine motor function in children. Our recent rodent studies established that elevated Mn exposure causes these impairments. Here, rats were exposed orally to 0, 25, or 50 mg Mn kg -1 day -1 during early postnatal life (PND 1-21) or lifelong to determine whether early life Mn exposure causes heightened behavioral reactivity in the open field, lasting changes in the catecholaminergic systems in the medial prefrontal cortex (mPFC), altered dendritic spine density, and whether lifelong exposure exacerbates these effects. We also assessed astrocyte reactivity (glial fibrillary acidic protein, GFAP), and astrocyte complement C3 and S100A10 protein levels as markers of A1 proinflammatory or A2 anti-inflammatory reactive astrocytes. Postnatal Mn exposure caused heightened behavioral reactivity during the first 5-10 min intervals of daily open field test sessions, consistent with impairments in arousal regulation. Mn exposure reduced the evoked release of norepinephrine (NE) and caused decreased protein levels of tyrosine hydroxylase (TH), dopamine (DA) and NE transporters, and DA D1 receptors, along with increased DA D2 receptors. Mn also caused a lasting increase in reactive astrocytes (GFAP) exhibiting increased A1 and A2 phenotypes, with a greater induction of the A1 proinflammatory phenotype. These results demonstrate that early life Mn exposure causes broad lasting hypofunctioning of the mPFC catecholaminergic systems, consistent with the impaired arousal regulation, attention, impulse control, and fine motor function reported in these animals, suggesting that mPFC catecholaminergic dysfunction may underlie similar impairments reported in Mn-exposed children.
(© 2019 International Society for Neurochemistry.)