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Marked attenuation of inflammatory mediator-induced C-fiber sensitization for mechanical and hypotonic stimuli in TRPV4-/- mice.
Mol Pain. 2007 Oct 29; 3:31.MP

Abstract

Inflammatory mediators can directly sensitize primary afferent nociceptors to mechanical and osmotic stimuli. Sensitized nociceptors have a lowered threshold of activation and increased spontaneous activity, which result in symptoms of hyperalgesia and pain, respectively. The transient receptor potential vanilloid 4 (TRPV4) ligand-gated ion channel has been implicated in the hyperalgesia for mechanical and osmotic stimuli associated with inflammatory states. To investigate whether TRPV4 directly contributes to the mechanisms of inflammatory mediator sensitization of C-fiber nociceptors, we compared the effect of the injection of simplified inflammatory soup (prostaglandin E2 and serotonin) into the mechanical receptive fields of C-fibers in TRPV4+/+ and TRPV4-/- mice in vivo. Following the injection of the soup, the percentage of C-fibers responding to a hypotonic stimulus and the magnitude of the response was significantly greater in TRPV4+/+ mice compared to TRPV4-/- mice. Moreover, in response to simplified inflammatory soup only C-fibers from TRPV4+/+ mice exhibited increased spontaneous activity and decreased mechanical threshold. These marked impairments in the response of C-fibers in TRPV4-/- mice demonstrate the importance of TRPV4 in nociceptor sensitization; we suggest that TRPV4, as TRPV1, underlies the nociceptive effects of multiple inflammatory mediators on primary afferent.

Authors+Show Affiliations

Department of Anatomy, Division of Neuroscience, University of California, San Francisco, CA 94143, USA. xiaojie.chen@ucsf.eduNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

17967183

Citation

Chen, Xiaojie, et al. "Marked Attenuation of Inflammatory Mediator-induced C-fiber Sensitization for Mechanical and Hypotonic Stimuli in TRPV4-/- Mice." Molecular Pain, vol. 3, 2007, p. 31.
Chen X, Alessandri-Haber N, Levine JD. Marked attenuation of inflammatory mediator-induced C-fiber sensitization for mechanical and hypotonic stimuli in TRPV4-/- mice. Mol Pain. 2007;3:31.
Chen, X., Alessandri-Haber, N., & Levine, J. D. (2007). Marked attenuation of inflammatory mediator-induced C-fiber sensitization for mechanical and hypotonic stimuli in TRPV4-/- mice. Molecular Pain, 3, 31.
Chen X, Alessandri-Haber N, Levine JD. Marked Attenuation of Inflammatory Mediator-induced C-fiber Sensitization for Mechanical and Hypotonic Stimuli in TRPV4-/- Mice. Mol Pain. 2007 Oct 29;3:31. PubMed PMID: 17967183.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Marked attenuation of inflammatory mediator-induced C-fiber sensitization for mechanical and hypotonic stimuli in TRPV4-/- mice. AU - Chen,Xiaojie, AU - Alessandri-Haber,Nicole, AU - Levine,Jon D, Y1 - 2007/10/29/ PY - 2007/06/11/received PY - 2007/10/29/accepted PY - 2007/10/31/pubmed PY - 2008/1/25/medline PY - 2007/10/31/entrez SP - 31 EP - 31 JF - Molecular pain JO - Mol Pain VL - 3 N2 - Inflammatory mediators can directly sensitize primary afferent nociceptors to mechanical and osmotic stimuli. Sensitized nociceptors have a lowered threshold of activation and increased spontaneous activity, which result in symptoms of hyperalgesia and pain, respectively. The transient receptor potential vanilloid 4 (TRPV4) ligand-gated ion channel has been implicated in the hyperalgesia for mechanical and osmotic stimuli associated with inflammatory states. To investigate whether TRPV4 directly contributes to the mechanisms of inflammatory mediator sensitization of C-fiber nociceptors, we compared the effect of the injection of simplified inflammatory soup (prostaglandin E2 and serotonin) into the mechanical receptive fields of C-fibers in TRPV4+/+ and TRPV4-/- mice in vivo. Following the injection of the soup, the percentage of C-fibers responding to a hypotonic stimulus and the magnitude of the response was significantly greater in TRPV4+/+ mice compared to TRPV4-/- mice. Moreover, in response to simplified inflammatory soup only C-fibers from TRPV4+/+ mice exhibited increased spontaneous activity and decreased mechanical threshold. These marked impairments in the response of C-fibers in TRPV4-/- mice demonstrate the importance of TRPV4 in nociceptor sensitization; we suggest that TRPV4, as TRPV1, underlies the nociceptive effects of multiple inflammatory mediators on primary afferent. SN - 1744-8069 UR - https://www.unboundmedicine.com/medline/citation/17967183/Marked_attenuation_of_inflammatory_mediator_induced_C_fiber_sensitization_for_mechanical_and_hypotonic_stimuli_in_TRPV4_/__mice_ L2 - https://journals.sagepub.com/doi/10.1186/1744-8069-3-31?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -