ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Golli myelin basic proteins regulate oligodendroglial progenitor cell migration through voltage-gated Ca2+ influx.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 64 citations in OpenAlex.
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- STIM Proteins: The Gas and Brake of Calcium Entry in Neurons.Neuroscience bulletin · 2025Review
- Generation and characterization of cerebellar granule neurons specific knockout mice of Golli-MBP.Transgenic research · 2024Article
- Novel Tools and Investigative Approaches for the Study of Oligodendrocyte Precursor Cells (NG2-Glia) in CNS Development and Disease.Frontiers in cellular neuroscience · 2021Article
- Neuron-oligodendroglia interactions: Activity-dependent regulation of cellular signaling.Neuroscience letters · 2020Review
- CaCellular and molecular neurobiology · 2019Review
- Cell migration promotes dynamic cellular interactions to control cerebral cortex morphogenesis.Nature reviews. Neuroscience · 2019Review
- Enhanced oligodendrocyte maturation and myelination in a mouse model of Timothy syndrome.Glia · 2018Article
- Muscarinic Receptor MThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Conditional Deletion of the L-Type Calcium Channel Cav1.2 in NG2-Positive Cells Impairs Remyelination in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Electric Signals Regulate the Directional Migration of Oligodendrocyte Progenitor Cells (OPCs) via β1 Integrin.International journal of molecular sciences · 2016Article
- Conditional Deletion of the L-Type Calcium Channel Cav1.2 in Oligodendrocyte Progenitor Cells Affects Postnatal Myelination in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Golli Myelin Basic Proteins Modulate Voltage-Operated Ca(++) Influx and Development in Cortical and Hippocampal Neurons.Molecular neurobiology · 2016Article
- 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
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- Myelin in cartilaginous fish.Brain research · 2016Review
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Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Migration of oligodendrocyte progenitor cells (OPCs) from proliferative zones to their final location in the brain is an essential step in nervous system development. Golli proteins, products of the myelin basic protein gene, can modulate voltage-gated Ca(2+) uptake in OPCs during process extension and retraction. Given the importance of process extension/retraction on movement, the consequences of golli expression on OPC migration were examined in vivo and in vitro using time-lapse imaging of isolated OPCs and acute brain slice preparations from golli KO and golli J37 overexpressing mice (JOE). The results indicated that golli stimulated migration, and this enhanced motility was associated with increases in the activity of voltage operated Ca(2+) channels (VOCCs). Activation of VOCCs by high K(+) resulted in a significant increase in the migration speed of JOE OPCs versus control cells and golli-mediated modulation of OPC migration disappeared in the presence of VOCC antagonists. During migration, OPCs generated Ca(2+) oscillations that were dependent on voltage-calcium influx and both the amplitude and frequency of these Ca(2+) transients correlated positively with the rate of cell movement under a variety of pharmacological treatments. The Ca(2+) transient amplitude and the rate of cell movement were significantly lower in KO cells and significantly higher in JOE cells suggesting that the presence of golli promotes OPC migration by increasing the size of voltage-mediated Ca(2+) oscillations. These data define a new molecule that regulates Ca(2+) homeostasis in OPCs, and are the first to demonstrate that voltage-gated Ca(2+) channels can regulate an OPC function, such as migration.
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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.