ArticleThe Journal of biological chemistry2009
Synthetic ciguatoxins selectively activate Nav1.8-derived chimeric sodium channels expressed in HEK293 cells.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 39 citations in OpenAlex.
- Mouse N2a Neuroblastoma Assay: Uncertainties and Comparison with Alternative Cell-Based Assays for Ciguatoxin Detection.Marine drugs · 2023Article
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- Sodium channels and pain: from toxins to therapies.British journal of pharmacology · 2018Review
- Biotechnological and Pharmacological Applications of Biotoxins and Other Bioactive Molecules from Dinoflagellates.Marine drugs · 2017Review
- Ladder-Shaped Ion Channel Ligands: Current State of Knowledge.Marine drugs · 2017Review
- An Updated Review of Ciguatera Fish Poisoning: Clinical, Epidemiological, Environmental, and Public Health Management.Marine drugs · 2017Review
- Multiple sodium channel isoforms mediate the pathological effects of Pacific ciguatoxin-1.Scientific reports · 2017Article
- 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.Assay and drug development technologies · 2016Article
- Total synthesis and related studies of large, strained, and bioactive natural products.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2016Review
- Ionic mechanisms of spinal neuronal cold hypersensitivity in ciguatera.The European journal of neuroscience · 2015Article
- Animal toxins influence voltage-gated sodium channel function.Handbook of experimental pharmacology · 2014Review
- Ciguatoxins activate specific cold pain pathways to elicit burning pain from cooling.The EMBO journal · 2012Article
- Neurotoxins and their binding areas on voltage-gated sodium channels.Frontiers in pharmacology · 2011Article
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Authors and funding
8 authors at 6 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The synthetic ciguatoxin CTX3C has been shown to activate tetrodotoxin (TTX)-sensitive sodium channels (Na(v)1.2, Na(v)1.4, and Na(v)1.5) by accelerating activation kinetics and shifting the activation curve toward hyperpolarization (Yamaoka, K., Inoue, M., Miyahara, H., Miyazaki, K., and Hirama, M. (2004) Br. J. Pharmacol. 142, 879-889). In this study, we further explored the effects of CTX3C on the TTX-resistant sodium channel Na(v)1.8. TTX-resistant channels have been shown to be involved in transducing pain and related sensations (Akopian, A. N., Sivilotti, L., and Wood, J. N. (1996) Nature 379, 257-262). Thus, we hypothesized that ciguatoxin-induced activation of the Na(v)1.8 current would account for the neurological symptoms of ciguatera poisoning. We found that 0.1 mum CTX3C preferentially affected the activation process of the Na(v)1.8 channel compared with those of the Na(v)1.2 and Na(v)1.4 channels. Importantly, without stimulation, 0.1 mum CTX3C induced a large leakage current (I (L)). The conductance of the I (L) calculated relative to the maximum conductance (G (max)) was 10 times larger than that of Na(v)1.2 or Na(v)1.4. To determine the molecular domain of Na(v)1.8 responsible for conferring higher sensitivity to CTX3C, we made two chimeric constructs from Na(v)1.4 and Na(v)1.8. Chimeras containing the N-terminal half of Na(v)1.8 exhibited a large response similar to wild-type Na(v)1.8, indicating that the region conferring high sensitivity to ciguatoxin action is located in the D1 or D2 domains.
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