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Contribution of TRPV1 to the bradykinin-evoked nociceptive behavior and excitation of cutaneous sensory neurons.
Neurosci Res. 2008 Nov; 62(3):168-75.NR

Abstract

Bradykinin (BK), a major inflammatory mediator, excites and sensitizes nociceptor neurons/fibers, thus evoking pain and hyperalgesia. The cellular signaling mechanisms underlying these actions have remained unsolved, especially in regard to the identity of channels that mediate acute excitation. Here, to clarify the contribution of transient receptor potential vanilloid 1 (TRPV1), a heat-sensitive ion channel, to the BK-evoked nociceptor excitation and pain, we examined the behavioral and physiological BK-responses in TRPV1-deficient (KO) mice. A nocifencive behavior after BK injection (100 pmol/site) into mouse sole was reduced in TRPV1-KO mice compared with wild-type (WT). A higher dose of BK (1 nmol/site), however, induced the response in TRPV1-KO mice indistinguishable from that in the WT. BK-evoked excitation of cutaneous C-fibers in TRPV1-KO mice was comparable to that in WT. BK clearly increased intracellular calcium in cultured dorsal root ganglion (DRG) neurons of TRPV1-KO mice, although the incidence of BK-sensitive neurons was reduced. BK has been reported to activate TRPA1 indirectly, yet a considerable part of BK-sensitive DRG neurons did not respond to a TRPA1 agonist, mustard oil. These results suggest that BK-evoked nociception/nociceptor response would not be simply explained by activation of TRPV1 and A1, and that BK-evoked nociceptor excitation would be mediated by several ionic mechanisms.

Authors+Show Affiliations

Department of Neuroscience II, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusa-ku, Nagoya, Aichi 464-8601, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18789982

Citation

Katanosaka, Kimiaki, et al. "Contribution of TRPV1 to the Bradykinin-evoked Nociceptive Behavior and Excitation of Cutaneous Sensory Neurons." Neuroscience Research, vol. 62, no. 3, 2008, pp. 168-75.
Katanosaka K, Banik RK, Giron R, et al. Contribution of TRPV1 to the bradykinin-evoked nociceptive behavior and excitation of cutaneous sensory neurons. Neurosci Res. 2008;62(3):168-75.
Katanosaka, K., Banik, R. K., Giron, R., Higashi, T., Tominaga, M., & Mizumura, K. (2008). Contribution of TRPV1 to the bradykinin-evoked nociceptive behavior and excitation of cutaneous sensory neurons. Neuroscience Research, 62(3), 168-75. https://doi.org/10.1016/j.neures.2008.08.004
Katanosaka K, et al. Contribution of TRPV1 to the Bradykinin-evoked Nociceptive Behavior and Excitation of Cutaneous Sensory Neurons. Neurosci Res. 2008;62(3):168-75. PubMed PMID: 18789982.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Contribution of TRPV1 to the bradykinin-evoked nociceptive behavior and excitation of cutaneous sensory neurons. AU - Katanosaka,Kimiaki, AU - Banik,Ratan Kumar, AU - Giron,Rocio, AU - Higashi,Tomohiro, AU - Tominaga,Makoto, AU - Mizumura,Kazue, Y1 - 2008/08/23/ PY - 2008/06/18/received PY - 2008/08/04/revised PY - 2008/08/05/accepted PY - 2008/9/16/pubmed PY - 2009/1/7/medline PY - 2008/9/16/entrez SP - 168 EP - 75 JF - Neuroscience research JO - Neurosci Res VL - 62 IS - 3 N2 - Bradykinin (BK), a major inflammatory mediator, excites and sensitizes nociceptor neurons/fibers, thus evoking pain and hyperalgesia. The cellular signaling mechanisms underlying these actions have remained unsolved, especially in regard to the identity of channels that mediate acute excitation. Here, to clarify the contribution of transient receptor potential vanilloid 1 (TRPV1), a heat-sensitive ion channel, to the BK-evoked nociceptor excitation and pain, we examined the behavioral and physiological BK-responses in TRPV1-deficient (KO) mice. A nocifencive behavior after BK injection (100 pmol/site) into mouse sole was reduced in TRPV1-KO mice compared with wild-type (WT). A higher dose of BK (1 nmol/site), however, induced the response in TRPV1-KO mice indistinguishable from that in the WT. BK-evoked excitation of cutaneous C-fibers in TRPV1-KO mice was comparable to that in WT. BK clearly increased intracellular calcium in cultured dorsal root ganglion (DRG) neurons of TRPV1-KO mice, although the incidence of BK-sensitive neurons was reduced. BK has been reported to activate TRPA1 indirectly, yet a considerable part of BK-sensitive DRG neurons did not respond to a TRPA1 agonist, mustard oil. These results suggest that BK-evoked nociception/nociceptor response would not be simply explained by activation of TRPV1 and A1, and that BK-evoked nociceptor excitation would be mediated by several ionic mechanisms. SN - 0168-0102 UR - https://www.unboundmedicine.com/medline/citation/18789982/Contribution_of_TRPV1_to_the_bradykinin_evoked_nociceptive_behavior_and_excitation_of_cutaneous_sensory_neurons_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0168-0102(08)00220-4 DB - PRIME DP - Unbound Medicine ER -