The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.
Hyperalgesic agents increase a tetrodotoxin-resistant Na+ current in nociceptors.
Open accessAbstract
Sensitization of primary afferent neurons underlies much of the pain and tenderness associated with tissue injury and inflammation. The increase in excitability is caused by chemical agents released at the site of injury. Because recent studies suggest that an increase in voltage-gated Na+ currents may underlie increases in neuronal excitability associated with injury, we have tested the hypothesis that a tetrodotoxin-resistant voltage-gated Na+ current (TTX-R INa), selectively expressed in a subpopulation of sensory neurons with properties of nociceptors, is a target for hyperalgesic agents. Our results indicate that three agents that produce tenderness or hyperalgesia in vivo, prostaglandin E2, adenosine, and serotonin, modulate TTX-R INa. These agents increase the magnitude of the current, shift its conductance-voltage relationship in a hyperpolarized direction, and increase its rate of activation and inactivation. In contrast, thromboxane B2, a cyclooxygenase product that does not produce hyperalgesia, did not affect TTX-R INa. These results suggest that modulation of TTX-R INa is a mechanism for sensitization of mammalian nociceptors.
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Cites
Peripheral and central mechanisms of cutaneous hyperalgesia
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Nerve growth factor contributes to the generation of inflammatory sensory hypersensitivity
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Peptides and the primary afferent nociceptor
Levine, J., Fields, H., & Basbaum, A. (1993) · The Journal of Neuroscience · doi:10.1523/jneurosci.13-06-02273.1993 · Cited by 485
Self-citationDevor, M., Govrin-Lippmann, R., & Angelides, K. (1993) · The Journal of Neuroscience · doi:10.1523/jneurosci.13-05-01976.1993 · Cited by 310
Three types of sodium channels in adult rat dorsal root ganglion neurons
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Excitation and sensitization of fine articular afferents from cat's knee joint by prostaglandin E2.
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Self-citationPrimary sensory neurones: Neurofilament, neuropeptides and conduction velocity
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Neuronal plasticity: Increasing the gain in pain
Woolf, C. J., & Salter, M. W. (2000) · Science · doi:10.1126/science.288.5472.1765 · Cited by 3,781
The induction of pain: an integrative review
Millan, M. J. (1999) · Progress in Neurobiology · doi:10.1016/s0301-0082(98)00048-3 · Cited by 1,774
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
Resurgence of sodium channel research
Goldin, A. L. (2001) · Annual Review of Physiology · doi:10.1146/annurev.physiol.63.1.871 · Cited by 688
Transcriptional and posttranslational plasticity and the generation of inflammatory pain
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Metadata
- Authors
- Gold, M. S., Reichling, D. B., Shuster, M. J., & Levine, J. D.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1996-02-06
- Volume
- 93
- Issue
- 3
- Pages
- 1108-1112
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W1978939719
- Cited by
- 668
- References
- 16
- FWCI
- 23.62
- Type
- journal article
- Language
- en
- Open access
- green
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- Gold, M. S., Reichling, D. B., Shuster, M. J., & Levine, J. D. (1996). Hyperalgesic agents increase a tetrodotoxin-resistant Na+ current in nociceptors. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.93.3.1108
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
