ArticleBiomolecules & therapeutics2018
T-Type Calcium Channels Are Required to Maintain Viability of Neural Progenitor Cells.
Article in Biomolecules & therapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- CaThe Journal of biological chemistry · 2025Article
- Evaluating chemical effects on human neural cells through calcium imaging and deep learning.iScience · 2024Article
- T-Type Voltage-Gated Calcium Channels: Potential Regulators of Smooth Muscle Contractility.International journal of molecular sciences · 2024Review
- Rare CACNA1H and RELN variants interact through mTORC1 pathway in oligogenic autism spectrum disorder.Translational psychiatry · 2022Article
- T-Type Calcium Channel Inhibitors Induce Apoptosis in Medulloblastoma Cells Associated with Altered Metabolic Activity.Molecular neurobiology · 2022Article
- Potential effects of commonly applied drugs on neural stem cell proliferation and viability: A hypothesis-generating systematic review and meta-analysis.Frontiers in molecular neuroscience · 2022Article
- Altered Expression of Ion Channels in White Matter Lesions of Progressive Multiple Sclerosis: What Do We Know About Their Function?Frontiers in cellular neuroscience · 2021Review
- Development of a High-throughput Agar Colony Formation Assay to Identify Drug Candidates against Medulloblastoma.Pharmaceuticals (Basel, Switzerland) · 2020Article
- Epigenetically Upregulated T-Type Calcium Channels Contribute to Abnormal Proliferation of Embryonic Neural Progenitor Cells Exposed to Valproic Acid.Biomolecules & therapeutics · 2020Article
- A rare CACNA1H variant associated with amyotrophic lateral sclerosis causes complete loss of CaMolecular brain · 2020Article
- Genetic T-type calcium channelopathies.Journal of medical genetics · 2020Review
- TAF1-gene editing alters the morphology and function of the cerebellum and cerebral cortex.Neurobiology of disease · 2019Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T-type calcium channels are low voltage-activated calcium channels that evoke small and transient calcium currents. Recently, T-type calcium channels have been implicated in neurodevelopmental disorders such as autism spectrum disorder and neural tube defects. However, their function during embryonic development is largely unknown. Here, we investigated the function and expression of T-type calcium channels in embryonic neural progenitor cells (NPCs). First, we compared the expression of T-type calcium channel subtypes (CaV3.1, 3.2, and 3.3) in NPCs and differentiated neural cells (neurons and astrocytes). We detected all subtypes in neurons but not in astrocytes. In NPCs, CaV3.1 was the dominant subtype, whereas CaV3.2 was weakly expressed, and CaV3.3 was not detected. Next, we determined CaV3.1 expression levels in the cortex during early brain development. Expression levels of CaV3.1 in the embryonic period were transiently decreased during the perinatal period and increased at postnatal day 11. We then pharmacologically blocked T-type calcium channels to determine the effects in neuronal cells. The blockade of T-type calcium channels reduced cell viability, and induced apoptotic cell death in NPCs but not in differentiated astrocytes. Furthermore, blocking T-type calcium channels rapidly reduced AKT-phosphorylation (Ser473) and GSK3β-phosphorylation (Ser9). Our results suggest that T-type calcium channels play essential roles in maintaining NPC viability, and T-type calcium channel blockers are toxic to embryonic neural cells, and may potentially be responsible for neurodevelopmental disorders.
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