ArticleNeurotoxicology2013
Manganese inhibits ATP-induced calcium entry through the transient receptor potential channel TRPC3 in astrocytes.
Article in Neurotoxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Evidence for a role of calcium and vitamin D in the regulation of manganese homeostasis and in the prevention or management of manganese-induced disease.American journal of physiology. Endocrinology and metabolism · 2026Article
- Exposure to manganese during juvenile development increases microglial activation in the hippocampus following systemic infection with A/California/04/2009 Influenza A H1N1 virus.Frontiers in toxicology · 2026Article
- Epitranscriptomic reader YTHDF2 regulates SEK1(iScience · 2024Article
- Mechanism of Gene-Environment Interactions Driving Glial Activation in Parkinson's Diseases.Current environmental health reports · 2021Review
- Critical Involvement of Glial Cells in Manganese Neurotoxicity.BioMed research international · 2021Review
- Mechanism of Manganese Dysregulation of Dopamine Neuronal Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Synchrotron radiation-based FTIR spectro-microscopy of the brainstem of the hSOD1 G93A rat model of amyotrophic lateral sclerosis.European biophysics journal : EBJ · 2019Article
- Transcriptome Analysis Reveals Distinct Responses to PhysiologicFrontiers in genetics · 2019Article
- Manganese exposure induces neuroinflammation by impairing mitochondrial dynamics in astrocytes.Neurotoxicology · 2018Article
- TRPC1- and TRPC3-dependent CaGlia · 2017Article
- Inflammatory Activation of Microglia and Astrocytes in Manganese Neurotoxicity.Advances in neurobiology · 2017Review
- "Manganese-induced neurotoxicity: a review of its behavioral consequences and neuroprotective strategies".BMC pharmacology & toxicology · 2016Review
- Potential Role of Epigenetic Mechanism in Manganese Induced Neurotoxicity.BioMed research international · 2016Review
- Glyphosate, pathways to modern diseases III: Manganese, neurological diseases, and associated pathologies.Surgical neurology international · 2015Article
- A zebrafish model of manganism reveals reversible and treatable symptoms that are independent of neurotoxicity.Disease models & mechanisms · 2014Article
- Article
- Dopaminergic neurotoxicants cause biphasic inhibition of purinergic calcium signaling in astrocytes.PloS one · 2014Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic exposure to elevated levels of manganese (Mn(2+)) causes neuronal injury and inflammatory activation of glia. Astrocytes selectively accumulate Mn(2+), which inhibits mitochondrial respiration and increases production of reactive oxygen species. We previously reported that sub-acute exposure to low micromolar levels of Mn(2+) in primary astrocytes inhibited ATP-induced calcium (Ca(2+)) signaling, associated with decreased levels of endoplasmic reticulum Ca(2+) and increased mitochondrial Ca(2+) loads. In the present studies, we postulated that the mechanism underlying the capacity of Mn(2+) to inhibit these purinergic signals in astrocytes could be due to competition with Ca(2+) for entry through a plasma membrane channel. These data demonstrate that acutely applied Mn(2+) rapidly inhibited ATP-induced Ca(2+) waves and transients in primary striatal astrocytes. Mn(2+) also decreased influx of extracellular Ca(2+) induced by 1-oleoyl-2-acetyl-sn-glycerol (OAG), a direct activator of the transient receptor potential channel, TRPC3. The TRPC3 inhibitor, pyrazole-3, prevented ATP- and OAG-dependent transport of Mn(2+) from extracellular stores, demonstrated by a dramatic reduction in the rate of fluorescence quenching of Fura-2. These data indicate that Mn(2+) can acutely inhibit ATP-dependent Ca(2+) signaling in astrocytes by blocking Ca(2+) entry through the receptor-operated cation channel, TRPC3. Loss of normal astrocytic responses to purinergic signals due to accumulation of Mn(2+) could therefore comprise critical homeostatic functions necessary for metabolic and trophic support of neurons.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.