ArticleFrontiers in cellular neuroscience2016
NSC-34 Motor Neuron-Like Cells Are Unsuitable as Experimental Model for Glutamate-Mediated Excitotoxicity.
Article in Frontiers in cellular neuroscience, 2016. 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, 51 citations in OpenAlex.
- Mitochondria-containing large extracellular vesicles target mouse motor neurons upon intramuscular injection.Extracellular vesicle · 2026Article
- Sustained CREB Phosphorylation Is Associated with Neuritogenic Prostanoid Signaling in NSC-34 Cells.Cells · 2026Article
- Stress exposure affects amyotrophic lateral sclerosis pathogenesis via PI3K/Akt and focal adhesion pathways: evidence from three experimental models.Scientific reports · 2025Article
- BV2 Microglial Cell Activation/Polarization Is Influenced by Extracellular Vesicles Released from Mutated SOD1 NSC-34 Motoneuron-like Cells.Biomedicines · 2024Article
- Mechanical scratch injury on differentiated motor neuron of NSC-34 cells as an in vitro model for evaluation of neuroregeneration potential of NeuroAiD II (MLC901).In vitro models · 2024Article
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- Neuroprotective effects of ellorarxine in neuronal models of degeneration.Frontiers in neuroscience · 2024Article
- Research Models to Study Ferroptosis's Impact in Neurodegenerative Diseases.Pharmaceutics · 2023Review
- Signatures in in vitro infection of NSC-34 mouse neurons and their cell nucleus with Rickettsia helvetica.BMC microbiology · 2023Article
- Optimization of Application-Driven Development ofTissue engineering. Part B, Reviews · 2022Review
- Present State and Future Perspectives of Prostaglandins as a Differentiation Factor in Motor Neurons.Cellular and molecular neurobiology · 2022Review
- TMEM63C mutations cause mitochondrial morphology defects and underlie hereditary spastic paraplegia.Brain : a journal of neurology · 2022Article
- Insights into the Critical Role of Exosomes in the Brain; from Neuronal Activity to Therapeutic Effects.Molecular neurobiology · 2022Review
- Formulation, Characterization, and Cytotoxicity Evaluation of Lactoferrin Functionalized Lipid Nanoparticles for Riluzole Delivery to the Brain.Pharmaceutics · 2022Article
- The Transcriptional Complex Sp1/KMT2A by Up-Regulating Restrictive Element 1 Silencing Transcription Factor Accelerates Methylmercury-Induced Cell Death in Motor Neuron-Like NSC34 Cells Overexpressing SOD1-G93A.Frontiers in neuroscience · 2021Article
- The overexpression of TDP-43 in astrocytes causes neurodegeneration via a PTP1B-mediated inflammatory response.Journal of neuroinflammation · 2020Article
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- Neuromuscular disease modeling on a chip.Disease models & mechanisms · 2020Review
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- Time-Course Changes and Role of Autophagy in Primary Spinal Motor Neurons Subjected to Oxygen-Glucose Deprivation: Insights Into Autophagy Changes in a Cellular Model of Spinal Cord Ischemia.Frontiers in cellular neuroscience · 2020Article
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glutamate-induced excitotoxicity is a major contributor to motor neuron degeneration in the pathogenesis of amyotrophic lateral sclerosis (ALS). The spinal cord × Neuroblastoma hybrid cell line (NSC-34) is often used as a bona fide cellular model to investigate the physiopathological mechanisms of ALS. However, the physiological response of NSC-34 to glutamate remains insufficiently described. In this study, we evaluated the relevance of differentiated NSC-34 (NSC-34D) as an in vitro model for glutamate excitotoxicity studies. NSC-34D showed morphological and physiological properties of motor neuron-like cells and expressed glutamate receptor subunits GluA1-4, GluN1 and GluN2A/D. Despite these diverse characteristics, no specific effect of glutamate was observed on cultured NSC-34D survival and morphology, in contrast to what has been described in primary culture of motor neurons (MN). Moreover, a small non sustained increase in the concentration of intracellular calcium was observed in NSC-34D after exposure to glutamate compared to primary MN. Our findings, together with the inability to obtain cultures containing only differentiated cells, suggest that the motor neuron-like NSC-34 cell line is not a suitable in vitro model to study glutamate-induced excitotoxicity. We suggest that the use of primary cultures of MN is more suitable than NSC-34 cell line to explore the pathogenesis of glutamate-mediated excitotoxicity at the cellular level in ALS and other motor neuron diseases.
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