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TRPA1 contributes to capsaicin-induced facial cold hyperalgesia in rats.
Eur J Oral Sci. 2014 Dec; 122(6):391-6.EJ

Abstract

Orofacial cold hyperalgesia is known to cause severe persistent pain in the face following trigeminal nerve injury or inflammation, and transient receptor potential (TRP) vanilloid 1 (TRPV1) and TRP ankylin 1 (TRPA1) are thought to be involved in cold hyperalgesia. However, how these two receptors are involved in cold hyperalgesia is not fully understood. To clarify the mechanisms underlying facial cold hyperalgesia, nocifensive behaviors to cold stimulation, the expression of TRPV1 and TRPA1 in trigeminal ganglion (TG) neurons, and TG neuronal excitability to cold stimulation following facial capsaicin injection were examined in rats. The head-withdrawal reflex threshold (HWRT) to cold stimulation of the lateral facial skin was significantly decreased following facial capsaicin injection. This reduction of HWRT was significantly recovered following local injection of TRPV1 antagonist as well as TRPA1 antagonist. Approximately 30% of TG neurons innervating the lateral facial skin expressed both TRPV1 and TRPA1, and about 64% of TRPA1-positive neurons also expressed TRPV1. The TG neuronal excitability to noxious cold stimulation was significantly increased following facial capsaicin injection and this increase was recovered by pretreatment with TRPA1 antagonist. These findings suggest that TRPA1 sensitization via TRPV1 signaling in TG neurons is involved in cold hyperalgesia following facial skin capsaicin injection.

Authors+Show Affiliations

Department of Physiology, Nihon University School of Dentistry, Tokyo, Japan; Department of Oral and Maxillofacial Surgery, Nihon University School of Dentistry, Tokyo, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

25371244

Citation

Honda, Kuniya, et al. "TRPA1 Contributes to Capsaicin-induced Facial Cold Hyperalgesia in Rats." European Journal of Oral Sciences, vol. 122, no. 6, 2014, pp. 391-6.
Honda K, Shinoda M, Furukawa A, et al. TRPA1 contributes to capsaicin-induced facial cold hyperalgesia in rats. Eur J Oral Sci. 2014;122(6):391-6.
Honda, K., Shinoda, M., Furukawa, A., Kita, K., Noma, N., & Iwata, K. (2014). TRPA1 contributes to capsaicin-induced facial cold hyperalgesia in rats. European Journal of Oral Sciences, 122(6), 391-6. https://doi.org/10.1111/eos.12157
Honda K, et al. TRPA1 Contributes to Capsaicin-induced Facial Cold Hyperalgesia in Rats. Eur J Oral Sci. 2014;122(6):391-6. PubMed PMID: 25371244.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - TRPA1 contributes to capsaicin-induced facial cold hyperalgesia in rats. AU - Honda,Kuniya, AU - Shinoda,Masamichi, AU - Furukawa,Akihiko, AU - Kita,Kozue, AU - Noma,Noboru, AU - Iwata,Koichi, Y1 - 2014/11/05/ PY - 2014/09/26/accepted PY - 2014/11/6/entrez PY - 2014/11/6/pubmed PY - 2015/11/5/medline KW - orofacial pain KW - transient receptor potential ankylin 1 KW - transient receptor potential vanilloid 1 KW - trigeminal ganglion SP - 391 EP - 6 JF - European journal of oral sciences JO - Eur J Oral Sci VL - 122 IS - 6 N2 - Orofacial cold hyperalgesia is known to cause severe persistent pain in the face following trigeminal nerve injury or inflammation, and transient receptor potential (TRP) vanilloid 1 (TRPV1) and TRP ankylin 1 (TRPA1) are thought to be involved in cold hyperalgesia. However, how these two receptors are involved in cold hyperalgesia is not fully understood. To clarify the mechanisms underlying facial cold hyperalgesia, nocifensive behaviors to cold stimulation, the expression of TRPV1 and TRPA1 in trigeminal ganglion (TG) neurons, and TG neuronal excitability to cold stimulation following facial capsaicin injection were examined in rats. The head-withdrawal reflex threshold (HWRT) to cold stimulation of the lateral facial skin was significantly decreased following facial capsaicin injection. This reduction of HWRT was significantly recovered following local injection of TRPV1 antagonist as well as TRPA1 antagonist. Approximately 30% of TG neurons innervating the lateral facial skin expressed both TRPV1 and TRPA1, and about 64% of TRPA1-positive neurons also expressed TRPV1. The TG neuronal excitability to noxious cold stimulation was significantly increased following facial capsaicin injection and this increase was recovered by pretreatment with TRPA1 antagonist. These findings suggest that TRPA1 sensitization via TRPV1 signaling in TG neurons is involved in cold hyperalgesia following facial skin capsaicin injection. SN - 1600-0722 UR - https://www.unboundmedicine.com/medline/citation/25371244/TRPA1_contributes_to_capsaicin_induced_facial_cold_hyperalgesia_in_rats_ L2 - https://doi.org/10.1111/eos.12157 DB - PRIME DP - Unbound Medicine ER -