ArticleNeurochemical research1996
Release of intracellular calcium stores leads to retraction of membrane sheets and cell death in mature mouse oligodendrocytes.
Article in Neurochemical research, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed.
- Cation Channel TMEM63A Autonomously Facilitates Oligodendrocyte Differentiation at an Early Stage.Neuroscience bulletin · 2025Article
- Adult-onset of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) syndrome with hypothyroidism and psychiatric disorders.eNeurologicalSci · 2017Article
- Intertwining extracellular nucleotides and their receptors with Ca2+ in determining adult neural stem cell survival, proliferation and final fate.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016Review
- Systematic Review of Pharmacological Properties of the Oligodendrocyte Lineage.Frontiers in cellular neuroscience · 2016Review
- Voltage-gated Ca2+ entry promotes oligodendrocyte progenitor cell maturation and myelination in vitro.Experimental neurology · 2015Article
- Article
- Golli myelin basic proteins regulate oligodendroglial progenitor cell migration through voltage-gated Ca2+ influx.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Article
- Increased expression of golli myelin basic proteins enhances calcium influx into oligodendroglial cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Cyclic GMP-dependent pathways protect differentiated oligodendrocytes from multiple types of injury.Neurochemical research · 2007Article
- Protection of mature oligodendrocytes by inhibitors of caspases and calpains.Neurochemical research · 2003Article
- Oligodendroglial response to the immune cytokine interferon gamma.Neurochemical research · 1999Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
The ability of mature oligodendrocytes (OLs) to recover from insult is important in repair of damage following demyelination. Since regulation of Ca2+ levels within cells plays a critical role in function and survival, this study investigates the effects of changes in cytoplasmic Ca2+ on the viability of cultured mouse OLs and their ability to maintain membrane sheets. Mature OLs in culture respond rapidly to the calcium ionophore A23187 and promptly return to resting Ca2+ levels when the ionophore is removed. Longer exposure to 0.1-1.0 microM A23187 leads to microtubule disruption, membrane sheet retraction and eventual cell death; nuclear lysis occurs in many of the OLs, as reported by Scolding, et al. (1) for rat OLs. In our cultures, mature OLs were more susceptible to nuclear lysis than were immature OLs or astroglia. Release of intracellular Ca2+ stores with thapsigargin at 5-10 microM also leads to retraction of membrane sheets. Following 6 hours of continuous exposure to thapsigargin, the effects on membrane sheets are reversed over the next 12 hours. After 18 hours of continuous exposure to thapsigargin, only occasional nuclear lysis is observed, but a number of the mature OLs show signs of DNA fragmentation, indicating that apoptotic death is occurring. Our results suggest that mature OLs cannot survive a prolonged influx of extracellular calcium as readily as immature OLs and astroglia, but have mechanism to withstand similar increases in cytoplasmic Ca2+ following sustained release of intracellular stores.
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Registered trials
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