The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Differential role of GDNF and NGF in the maintenance of two TTX-resistant sodium channels in adult DRG neurons
Open accessAbstract
Following sciatic nerve transection, the electrophysiological properties of small dorsal root ganglion (DRG) neurons are markedly altered, with attenuation of TTX-R sodium currents and the appearance of rapidly repriming TTX-S currents. The reduction in TTX-R currents has been attributed to a down-regulation of sodium channels SNS/PN3 and NaN. While infusion of exogenous NGF to the transected nerve restores SNS/PN3 transcripts to near-normal levels in small DRG neurons, TTX-R sodium currents are only partially rescued. Binding of the isolectin IB4 distinguishes two subpopulations of small DRG neurons: IB4+ neurons, which express receptors for the GDNF family of neurotrophins, and IB4- neurons that predominantly express TrkA. We show here that SNS/PN3 is expressed in approximately one-half of both IB4+ and IB4- DRG neurons, while NaN is preferentially expressed in IB4+ neurons. Whole-cell patch-clamp studies demonstrate that TTX-R sodium currents in IB4+ neurons have a more hyperpolarized voltage-dependence of activation and inactivation than do IB4- neurons, suggesting different electrophysiological properties for SNS/PN3 and NaN. We confirm that NGF restores SNS/PN3 mRNA levels in DRG neurons in vitro and demonstrate that the trk antagonist K252a blocks this rescue. The down-regulation of NaN mRNA is, nevertheless, not rescued by NGF-treatment in either IB4+ or IB4- neurons and NGF-treatment in vitro does not significantly increase the peak amplitude of the TTX-R current in small DRG neurons. In contrast, GDNF-treatment causes a twofold increase in the peak amplitude of TTX-R sodium currents and restores both SNS/PN3 and NaN mRNA to near-normal levels in IB4+ neurons. These observations provide a mechanism for the partial restoration of TTX-R sodium currents by NGF in axotomized DRG neurons, and demonstrate that the neurotrophins NGF and GDNF differentially regulate sodium channels SNS/PN3 and NaN.
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Cites
Protection and repair of the nigrostriatal dopaminergic system by GDNF in vivo
Tomac, A., Lindqvist, E., Lin, L.-F. H., Ögren, S. O., Young, D., Hoffer, B. J., & Olson, L. (1995) · Nature · doi:10.1038/373335a0 · Cited by 1,079
Woolf, C. J. (1996) · Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences · doi:10.1098/rstb.1996.0040 · Cited by 218
Cited by
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-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-citationNaN/Nav1.9: a sodium channel with unique properties
Dib-Hajj, S., Black, J. A., Cummins, T. R., & Waxman, S. G. (2002) · Trends in Neurosciences · doi:10.1016/s0166-2236(02)02150-1 · Cited by 254
Self-citationBeyak, M. J., & Vanner, S. (2005) · Neurogastroenterology & Motility · doi:10.1111/j.1365-2982.2004.00596.x · Cited by 121
Metadata
- Authors
- Fjell, J., Cummins, T. R., Dib-Hajj, S. D., Fried, K., Black, J. A., & Waxman, S. G.
- Venue
- Molecular Brain Research
- Publisher
- Elsevier BV
- Published
- 1999-04
- Volume
- 67
- Issue
- 2
- Pages
- 267-282
- ISSN
- 0169-328X (ISSN-L)
- OpenAlex
- W2061135681
- Cited by
- 207
- References
- 2
- FWCI
- 5.04
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Fjell, J., Cummins, T. R., Dib-Hajj, S. D., Fried, K., Black, J. A., & Waxman, S. G. (1999). Differential role of GDNF and NGF in the maintenance of two TTX-resistant sodium channels in adult DRG neurons. Molecular Brain Research. https://doi.org/10.1016/s0169-328x(99)00070-4
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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