ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Multiple kinase pathways regulate voltage-dependent Ca2+ influx and migration in oligodendrocyte precursor cells.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 58 citations in OpenAlex.
- Mechanisms underlying spontaneous and evoked calcium responses in oligodendrocyte precursor cells: A modeling investigation.PLoS computational biology · 2026Article
- Voltage-Gated and Chemogenetic Modulation of Calcium Signaling in Oligodendrocyte Development and Synaptic Integration.Journal of neurochemistry · 2025Review
- Roles of Ion Channels in Oligodendrocyte Precursor Cells: From Physiology to Pathology.International journal of molecular sciences · 2025Review
- Norepinephrine modulates calcium dynamics in cortical oligodendrocyte precursor cells promoting proliferation during arousal in mice.Nature neuroscience · 2023Article
- Recent Insights into the Functional Role of AMPA Receptors in the Oligodendrocyte Lineage Cells In Vivo.International journal of molecular sciences · 2023Review
- Ion Channels as New Attractive Targets to Improve Re-Myelination Processes in the Brain.International journal of molecular sciences · 2021Review
- Manipulating oligodendrocyte intrinsic regeneration mechanism to promote remyelination.Cellular and molecular life sciences : CMLS · 2021Review
- Glutamate Signaling via the AMPAR Subunit GluR4 Regulates Oligodendrocyte Progenitor Cell Migration in the Developing Spinal Cord.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- L-Type CaFrontiers in cell and developmental biology · 2021Article
- Deletion of Voltage-Gated Calcium Channels in Astrocytes during Demyelination Reduces Brain Inflammation and Promotes Myelin Regeneration in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- CaCellular and molecular neurobiology · 2019Review
- Enhanced oligodendrocyte maturation and myelination in a mouse model of Timothy syndrome.Glia · 2018Article
- Article
- TRPV4 is functionally expressed in oligodendrocyte precursor cells and increases their proliferation.Pflugers Archiv : European journal of physiology · 2018Article
- Dynamic Calcium Release From Endoplasmic Reticulum Mediated by Ryanodine Receptor 3 Is Crucial for Oligodendroglial Differentiation.Frontiers in molecular neuroscience · 2018Article
- Novel calcium-related targets of insulin in hippocampal neurons.Neuroscience · 2017Article
- 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
- 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
- Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
It is becoming increasingly clear that voltage-operated Ca(2+) channels (VOCCs) play a fundamental role in the development of oligodendrocyte progenitor cells (OPCs). Because direct phosphorylation by different kinases is one of the most important mechanisms involved in VOCC modulation, the aim of this study was to evaluate the participation of serine-threonine kinases and tyrosine kinases (TKs) on Ca(2+) influx mediated by VOCCs in OPCs. Calcium imaging revealed that OPCs exhibited Ca(2+) influx after plasma membrane depolarization via L-type VOCCs. Furthermore, VOCC-mediated Ca(2+) influx declined with OPC differentiation, indicating that VOCCs are developmentally regulated in OPCs. PKC activation significantly increased VOCC activity in OPCs, whereas PKA activation produced the opposite effect. The results also indicated that OPC morphological changes induced by PKC activation were partially mediated by VOCCs. Our data clearly suggest that TKs exert an activating influence on VOCC function in OPCs. Furthermore, using the PDGF response as a model to probe the role of TK receptors (TKr) on OPC Ca(2+) uptake, we found that TKr activation potentiated Ca(2+) influx after membrane depolarization. Interestingly, this TKr modulation of VOCCs appeared to be essential for the PDGF enhancement of OPC migration rate, because cell motility was completely blocked by TKr antagonists, as well as VOCC inhibitors, in migration assays. The present study strongly demonstrates that PKC and TKrs enhance Ca(2+) influx induced by depolarization in OPCs, whereas PKA has an inhibitory effect. These kinases modulate voltage-operated Ca(2+) uptake in OPCs and participate in the modulation of process extension and 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.