The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.
A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons
Abstract
Disease-producing mutations of ion channels are usually characterized as producing hyperexcitability or hypoexcitability. We show here that a single mutation can produce hyperexcitability in one neuronal cell type and hypoexcitability in another neuronal cell type. We studied the functional effects of a mutation of sodium channel Na v 1.7 associated with a neuropathic pain syndrome, erythermalgia, within sensory and sympathetic ganglion neurons, two cell types where Na v 1.7 is normally expressed. Although this mutation depolarizes resting membrane potential in both types of neurons, it renders sensory neurons hyperexcitable and sympathetic neurons hypoexcitable. The selective presence, in sensory but not sympathetic neurons, of the Na v 1.8 channel, which remains available for activation at depolarized membrane potentials, is a major determinant of these opposing effects. These results provide a molecular basis for the sympathetic dysfunction that has been observed in erythermalgia. Moreover, these findings show that a single ion channel mutation can produce opposing phenotypes (hyperexcitability or hypoexcitability) in the different cell types in which the channel is expressed.
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Cites
A tetrodotoxin-resistant voltage-gated sodium channel expressed by sensory neurons
Akopian, A. N., Sivilotti, L., & Wood, J. N. (1996) · Nature · doi:10.1038/379257a0 · Cited by 1,103
Mutations in SCN9A, encoding a sodium channel alpha subunit, in patients with primary erythermalgia
Yang, Y., Wang, Y., Li, S., Xu, Z., Li, H., Ma, L., Fan, J., Bu, D., Liu, B., Fan, Z., et al. (2004) · Journal of Medical Genetics · doi:10.1136/jmg.2003.012153 · Cited by 801
Contribution of Nav1.8 Sodium Channels to Action Potential Electrogenesis in DRG Neurons
Renganathan, M., Cummins, T. R., & Waxman, S. G. (2001) · Journal of Neurophysiology · doi:10.1152/jn.2001.86.2.629 · Cited by 566
Self-citationToledo-Aral, J. J., Moss, B. L., He, Z.-J., Koszowski, A. G., Whisenand, T., Levinson, S. R., Wolf, J. J., Silos-Santiago, I., Halegoua, S., & Mandel, G. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.4.1527 · Cited by 525
Cummins, T. R., & Waxman, S. G. (1997) · The Journal of Neuroscience · doi:10.1523/jneurosci.17-10-03503.1997 · Cited by 520
Self-citationDib-Hajj, S. D., Tyrrell, L., Black, J. A., & Waxman, S. G. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.15.8963 · Cited by 503
Self-citationGain-of-function mutation in Nav1.7 in familial erythromelalgia induces bursting of sensory neurons
Dib-Hajj, S. D., Rush, A. M., Cummins, T. R., Hisama, F. M., Novella, S., Tyrrell, L., Marshall, L., & Waxman, S. G. (2005) · Brain · doi:10.1093/brain/awh514 · Cited by 490
Self-citationSangameswaran, L., Delgado, S. G., Fish, L. M., Koch, B. D., Jakeman, L. B., Stewart, G. R., Sze, P., Hunter, J. C., Eglen, R. M., & Herman, R. C. (1996) · Journal of Biological Chemistry · doi:10.1074/jbc.271.11.5953 · Cited by 432
Blair, N. T., & Bean, B. P. (2002) · The Journal of Neuroscience · doi:10.1523/jneurosci.22-23-10277.2002 · Cited by 426
Electrophysiological Properties of Mutant Na v 1.7 Sodium Channels in a Painful Inherited Neuropathy
Cummins, T. R., Dib-Hajj, S. D., & Waxman, S. G. (2004) · The Journal of Neuroscience · doi:10.1523/jneurosci.2695-04.2004 · Cited by 394
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Cited by
Mechanisms of neuropathic pain
Campbell, J. N., & Meyer, R. A. (2006) · Neuron · doi:10.1016/j.neuron.2006.09.021 · Cited by 1,471
The Role of Voltage-Gated Sodium Channels in Pain Signaling
Bennett, D. L., Clark, A. J., Huang, J., Waxman, S. G., & Dib-Hajj, S. D. (2019) · Physiological Reviews · doi:10.1152/physrev.00052.2017 · Cited by 730
Self-citationThe roles of sodium channels in nociception: Implications for mechanisms of pain
Cummins, T. R., Sheets, P. L., & Waxman, S. G. (2007) · Pain · doi:10.1016/j.pain.2007.07.026 · Cited by 485
Self-citationMultiple sodium channels and their roles in electrogenesis within dorsal root ganglion neurons
Rush, A. M., Cummins, T. R., & Waxman, S. G. (2007) · The Journal of Physiology · doi:10.1113/jphysiol.2006.121483 · Cited by 425
Self-citationSodium channel SCN1A and epilepsy: Mutations and mechanisms
Escayg, A., & Goldin, A. L. (2010) · Epilepsia · doi:10.1111/j.1528-1167.2010.02640.x · Cited by 398
Metadata
- Authors
- Rush, A. M., Dib-Hajj, S. D., Liu, S., Cummins, T. R., Black, J. A., & Waxman, S. G.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2006-05-23
- Volume
- 103
- Issue
- 21
- Pages
- 8245-8250
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2050910050
- Cited by
- 408
- References
- 31
- FWCI
- 11.42
- Type
- journal article
- Language
- en
- Open access
- closed
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