The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
GTP-induced tetrodotoxin-resistant Na+ current regulates excitability in mouse and rat small diameter sensory neurones
Open accessAbstract
Peripheral pain thresholds are regulated by the actions of inflammatory mediators. Some act through G-protein-coupled receptors on voltage-gated sodium channels. We have found that a low-threshold, persistent tetrodotoxin-resistant Na+ current, attributed to NaV1.9, is upregulated by GTP and its non-hydrolysable analogue GTP-gamma-S, but not by GDP. Inclusion of GTP-gamma-S (500 microM) in the internal solution led to an increase in maximal current amplitude of > 300 % within 5 min. In current clamp, upregulation of persistent current was associated with a more negative threshold for action potential induction (by 15-16 mV) assessed from a holding potential of -90 mV. This was not seen in neurones without the low-threshold current or with internal GDP (P < 0.001). In addition, persistent current upregulation depolarized neurones. At -60 mV, internal GTP-gamma-S led to the generation of spontaneous activity in initially silent neurones only when persistent current was upregulated. These findings suggest that regulation of the persistent current has important consequences for nociceptor excitability.
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Cites
Postsynaptic induction of BDNF-mediated long-term potentiation
Kovalchuk, Y., Hanse, E., Kafitz, K. W., & Konnerth, A. (2002) · Science · doi:10.1126/science.1067766 · Cited by 456
Neurotrophin-evoked depolarization requires the sodium channel NaV1.9
Blum, R., Kafitz, K. W., & Konnerth, A. (2002) · Nature · doi:10.1038/nature01085 · Cited by 266
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-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 Channels and Mechanisms of Neuropathic Pain
Devor, M. (2006) · The Journal of Pain · doi:10.1016/j.jpain.2005.09.006 · Cited by 401
From modulator to mediator: rapid effects of BDNF on ion channels
Rose, C. R., Blum, R., Kafitz, K. W., Kovalchuk, Y., & Konnerth, A. (2004) · BioEssays · doi:10.1002/bies.20118 · Cited by 106
Metadata
- Authors
- Baker, M. D., Chandra, S. Y., Ding, Y., Waxman, S. G., & Wood, J. N.
- Venue
- The Journal of Physiology
- Publisher
- Wiley
- Published
- 2003-04
- Volume
- 548
- Issue
- 2
- Pages
- 373-382
- ISSN
- 0022-3751 (ISSN-L)
- 1469-7793
- OpenAlex
- W2102671024
- Cited by
- 183
- References
- 2
- FWCI
- 4.07
- Type
- journal article
- Language
- en
- Open access
- green
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- Baker, M. D., Chandra, S. Y., Ding, Y., Waxman, S. G., & Wood, J. N. (2003). GTP-induced tetrodotoxin-resistant Na+ current regulates excitability in mouse and rat small diameter sensory neurones. The Journal of Physiology. https://doi.org/10.1111/j.1469-7793.2003.00373.x
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