ArticleAssay and drug development technologies2016
Characterization of Endogenous Sodium Channels in the ND7-23 Neuroblastoma Cell Line: Implications for Use as a Heterologous Ion Channel Expression System Suitable for Automated Patch Clamp Screening.
Article in Assay and drug development technologies, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Nociceptor sodium channels shape subthreshold phase, upstroke, and shoulder of action potentials.The Journal of general physiology · 2025Article
- Enhanced motivated behavior mediated by pharmacological targeting of the FGF14/NaNature communications · 2025Article
- Regulation of voltage-gated sodium channels by TNF-α during herpes simplex virus latency establishment.Journal of neurovirology · 2024Article
- Molecular and cellular context influences SCN8A variant function.JCI insight · 2024Article
- Development of ASIC1a ligand-gated ion channel drug screening assays across multiple automated patch clamp platforms.Frontiers in molecular neuroscience · 2022Article
- A Novel Spider Toxin Inhibits Fast Inactivation of the NaFrontiers in pharmacology · 2021Article
- Neurotoxicity of Tityus bahiensis (brown scorpion) venom in sympathetic vas deferens preparations and neuronal cells.Archives of toxicology · 2020Article
- Article
- The voltage-gated sodium channel inhibitor, 4,9-anhydrotetrodotoxin, blocks human NaNeuroscience letters · 2020Article
- Immortalized Dorsal Root Ganglion Neuron Cell Lines.Frontiers in cellular neuroscience · 2020Review
- Differential Inhibition of Neuronal Sodium Channel Subtypes by the General Anesthetic Isoflurane.The Journal of pharmacology and experimental therapeutics · 2019Article
- NaV1.6 and NaV1.7 channels are major endogenous voltage-gated sodium channels in ND7/23 cells.PloS one · 2019Article
- Modulatory effects of bufalin, an active ingredient from toad venom on voltage-gated sodium channels.Molecular biology reports · 2018Article
- Heat-resistant action potentials require TTX-resistant sodium channels NaThe Journal of general physiology · 2018Article
- A Chimeric NaV1.8 Channel Expression System Based on HEK293T Cell Line.Frontiers in pharmacology · 2018Article
- Differential binding of tetrodotoxin and its derivatives to voltage-sensitive sodium channel subtypes (NaBritish journal of pharmacology · 2017Article
- Electrophysiological and Pharmacological Analyses of NaFrontiers in pharmacology · 2017Article
- Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The rodent neuroblastoma cell line, ND7-23, is used to express voltage-dependent sodium (Nav) and other neuronal ion channels resistant to heterologous expression in Chinese hamster ovary (CHO) or human embryonic kidney (HEK) cells. Their advantage is that they provide endogenous factors and signaling pathways to promote ion channel peptide folding, expression, and function at the cell surface and are also amenable to automated patch clamping. However, ND7-23 cells exhibit endogenous tetrodotoxin (TTX)-sensitive Nav currents, and molecular profiling has revealed the presence of Nav1.2, Nav1.3, Nav1.6, and Nav1.7 transcripts, but no study has determined which subtypes contribute to functional channels at the cell surface. We profiled the repertoire of functional Nav channels endogenously expressed in ND7-23 cells using the QPatch automated patch clamp platform and selective toxins and small molecules. The potency and subtype selectivity of the ligands (Icagen compound 68 from patent US-20060025415-A1-20060202, 4,9 anhydro TTX, and Protoxin-II) were established in human Nav1.3, Nav1.6, and Nav1.7 channel cell lines before application of selective concentrations to ND7-23 cells. Our data confirm previous studies that >97% of macroscopic Nav current in ND7-23 cells is carried by TTX-sensitive channels (300 nM TTX) and that Nav1.7 is the predominant channel contributing to this response (65% of peak inward current), followed by Nav1.6 (∼20%) and negligible Nav1.3 currents (∼2%). In addition, our data are the first to assess the Nav1.6 potency (50% inhibitory concentration [IC50] of 33 nM) and selectivity (50-fold over Nav1.7) of 4,9 anhydro TTX in human Nav channels expressed in mammalian cells, confirming previous studies of rodent Nav channels expressed in oocytes and HEK cells.
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