期刊论文详细信息
NEUROSCIENCE LETTERS 卷:742
Acute 2,3,7,8-Tetrachlorodibenzo-p-dioxin exposure in adult mice does not alter the morphology or inflammatory response of cortical microglia
Article
Lowery, R. L.1  Latchney, S. E.2  Peer, R. P.1,6  Lamantia, C. E.1  Opanashuk, L.3  McCall, M.4,5  Majewska, A. K.1 
[1] Univ Rochester, Ctr Visual Sci, Dept Neurosci, Rochester, NY 14642 USA
[2] St Marys Coll Maryland, Biol Dept, St Marys City, MD 20686 USA
[3] Natl Inst Aging, Bethesda, MD 20892 USA
[4] Univ Rochester, Dept Biostat & Computat Biol, Rochester, NY 14642 USA
[5] Univ Rochester, Dept Biomed Genet, Rochester, NY 14642 USA
[6] Univ Rochester, Sch Med & Dent, Rochester, NY 14642 USA
关键词: Dioxin;    Aryl hydrocarbon receptor;    Microglia;    Neurotoxicity;    Visual cortex;   
DOI  :  10.1016/j.neulet.2020.135516
来源: Elsevier
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【 摘 要 】

Microglia, the immune cells of the brain, have a canonical role in regulating responses to neurological disease or injury, but have also recently been implicated as regulators of neumphysiological processes such as learning and memory. Given these dual immune and physiological roles, microglia are a likely mechanism by which external toxic stimuli are converted into deficits in neuronal circuitry and subsequently function. However, while it is well established that exposure to environmental toxicants negatively affects the peripheral immune system, it remains unknown whether and how such exposure causes neuroinflammation which, in turn, may negatively impact microglial functions in vivo. Here, we examined how acute 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure in adulthood, which negatively impacts immune cells in the periphery, affects micmglial characteristics in the cortex of the mouse. We found that microglia density, distribution, morphology, inflammatory signaling, and response to a secondary, pathological activation were unaffected by acute TCDD exposure. These results suggest that acute, peripheral TCDD exposure in adulthood is not sufficient to induce an overt inflammatory phenotype in cortical microglia.

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