The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.
Selective Blockade of the Capsaicin Receptor TRPV1 Attenuates Bone Cancer Pain
Open accessAbstract
Cancer colonization of bone leads to the activation of osteoclasts, thereby producing local tissue acidosis and bone resorption. This process may contribute to the generation of both ongoing and movement-evoked pain, resulting from the activation of sensory neurons that detect noxious stimuli (nociceptors). The capsaicin receptor TRPV1 (transient receptor potential vanilloid subtype 1) is a cation channel expressed by nociceptors that detects multiple pain-producing stimuli, including noxious heat and extracellular protons, raising the possibility that it is an important mediator of bone cancer pain via its capacity to detect osteoclast- and tumor-mediated tissue acidosis. Here, we show that TRPV1 is present on sensory neuron fibers that innervate the mouse femur and that, in an in vivo model of bone cancer pain, acute or chronic administration of a TRPV1 antagonist or disruption of the TRPV1 gene results in a significant attenuation of both ongoing and movement-evoked nocifensive behaviors. Administration of the antagonist had similar efficacy in reducing early, moderate, and severe pain-related responses, suggesting that TRPV1 may be a novel target for pharmacological treatment of chronic pain states associated with bone cancer metastasis.
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Citations
Cites
The capsaicin receptor: a heat-activated ion channel in the pain pathway
Caterina, M. J., Schumacher, M. A., Tominaga, M., Rosen, T. A., Levine, J. D., & Julius, D. (1997) · Nature · doi:10.1038/39807 · Cited by 9,107
Self-citationNeuronal 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 · cited 1×
“In addition to agents that can directly activate TRPV1, other factors such as bradykinin, ATP, and NGF can modulate TRPV1 function indirectly via activation of second-messenger signaling pathways (Woolf and Salter, 2000; Julius and Basbaum, 2001), resulting in TRPV1 sensitization.”
BackgroundImpaired nociception and pain sensation in mice lacking the capsaicin receptor
Caterina, M. J., Leffler, A., Malmberg, A. B., Martin, W. J., Trafton, J., Petersen-Zeitz, K. R., Koltzenburg, M., Basbaum, A. I., & Julius, D. (2000) · Science · doi:10.1126/science.288.5464.306 · Cited by 3,544
Self-citationThe Cloned Capsaicin Receptor Integrates Multiple Pain-Producing Stimuli
Tominaga, M., Caterina, M. J., Malmberg, A. B., Rosen, T. A., Gilbert, H., Skinner, K., Raumann, B. E., Basbaum, A. I., & Julius, D. (1998) · Neuron · doi:10.1016/s0896-6273(00)80564-4 · Cited by 3,081
Self-citationMolecular mechanisms of nociception
Julius, D., & Basbaum, A. I. (2001) · Nature · doi:10.1038/35093019 · Cited by 2,685 · cited 2×
“…- induced pain behaviors is that other receptors ( such as bradykinin , P2X 3 , and prostaglandin receptors , or acid - sensing ion channel 3 and voltage - gated sodium channels ) may also be involved in the generation and maintenance of this pain state ( Julius and Basbaum , 2001 ; Mantyh et al .”
BackgroundSelf-citationInduction of c-fos-like protein in spinal cord neurons following sensory stimulation
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Vanilloid receptor-1 is essential for inflammatory thermal hyperalgesia
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Cited by
Cancer pain and its impact on diagnosis, survival and quality of life
Mantyh, P. W. (2006) · Nature Reviews Neuroscience · doi:10.1038/nrn1914 · Cited by 441
Self-citationPrevarskaya, N., Zhang, L., & Barritt, G. (2007) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2007.05.006 · Cited by 355
The cannabinoid system and pain
Woodhams, S. G., Chapman, V., Finn, D. P., Hohmann, A. G., & Neugebauer, V. (2017) · Neuropharmacology · doi:10.1016/j.neuropharm.2017.06.015 · Cited by 267
The transient receptor potential vanilloid-1 channel in thermoregulation: a thermosensor it is not
Romanovsky, A. A., Almeida, M. C., Garami, A., Steiner, A. A., Norman, M. H., Morrison, S. F., Nakamura, K., Burmeister, J. J., & Nucci, T. B. (2009) · Pharmacological Reviews · doi:10.1124/pr.109.001263 · Cited by 253
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Metadata
- Authors
- Ghilardi, J. R., Röhrich, H., Lindsay, T. H., Sevcik, M. A., Schwei, M. J., Kubota, K., Halvorson, K. G., Poblete, J., Chaplan, S. R., Dubin, A. E., Carruthers, N. I., Swanson, D., Kuskowski, M., Flores, C. M., Julius, D., & Mantyh, P. W.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2005-03-23
- Volume
- 25
- Issue
- 12
- Pages
- 3126-3131
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2164144654
- Cited by
- 384
- References
- 34
- FWCI
- 9.31
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Ghilardi, J. R., Röhrich, H., Lindsay, T. H., Sevcik, M. A., Schwei, M. J., Kubota, K., Halvorson, K. G., Poblete, J., Chaplan, S. R., Dubin, A. E., Carruthers, N. I., Swanson, D., Kuskowski, M., Flores, C. M., Julius, D., & Mantyh, P. W. (2005). Selective Blockade of the Capsaicin Receptor TRPV1 Attenuates Bone Cancer Pain. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.3815-04.2005
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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.