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Updated: Feb 23, 2026
Microglia as a Surrogate Biosensor to Determine Nanoparticle Neurotoxicity
Published on: October 25, 2016
Inflammatory Activation of Microglia and Astrocytes in Manganese Neurotoxicity
Ronald B Tjalkens1,2,3, Katriana A Popichak4, Kelly A Kirkley5,6
1Program in Cell and Molecular Biology, Colorado State University, Fort Collins, CO, 80523-1680, USA. Ron.Tjalkens@colostate.edu.
Abstract:
Neurotoxicity due to excessive exposure to manganese (Mn) has been described as early as 1837 (Couper, Br Ann Med Pharm Vital Stat Gen Sci 1:41-42, 1837). Extensive research over the past two decades has revealed that Mn-induced neurological injury involves complex pathophysiological signaling mechanisms between neurons and glial cells. Glial cells are an important target of Mn in the brain, both for sequestration of the metal, as well as for activating inflammatory signaling pathways that damage neurons through overproduction of numerous reactive oxygen and nitrogen species and inflammatory cytokines. Understanding how these pathways are regulated in glial cells during Mn exposure is critical to determining the mechanisms underlying permanent neurological dysfunction stemming from excess exposure. The subject of this review will be to delineate mechanisms by which Mn interacts with glial cells to perturb neuronal function, with a particular emphasis on neuroinflammation and neuroinflammatory signaling between distinct populations of glial cells.
Insights
Excessive manganese (Mn) exposure causes neurotoxicity by affecting glial cells, which trigger inflammatory responses damaging neurons. Understanding these Mn-glial cell interactions is key to preventing permanent neurological dysfunction.
Area of Science:
- Neuroscience
- Toxicology
- Cell Biology
Background:
- Manganese (Mn) neurotoxicity has been recognized since the 19th century.
- Recent research highlights complex signaling between neurons and glial cells in Mn-induced neurological injury.
- Glial cells are primary targets for Mn, involved in metal sequestration and initiating inflammatory pathways.
Purpose of the Study:
- To delineate the mechanisms by which manganese interacts with glial cells.
- To emphasize the role of neuroinflammation and glial cell signaling in manganese neurotoxicity.
- To understand how glial cell pathways are regulated during manganese exposure.
Main Methods:
- Review of existing literature on manganese neurotoxicity.
- Analysis of signaling pathways between neurons and glial cells.
- Focus on neuroinflammatory responses in glial cells.
Main Results:
- Manganese exposure activates glial cells to produce reactive oxygen and nitrogen species.
- Glial cells release inflammatory cytokines that contribute to neuronal damage.
- Dysregulation of glial cell pathways is central to manganese-induced neurotoxicity.
Conclusions:
- Manganese-induced neurotoxicity involves intricate glial cell-mediated inflammatory signaling.
- Targeting glial cell inflammatory pathways may offer therapeutic strategies for manganese neurotoxicity.
- Further understanding of Mn-glial cell interactions is crucial for preventing neurological dysfunction.
