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Activation of transient receptor potential ankyrin 1 evokes nociception through substance P release from primary sensory neurons.
J Neurochem. 2012 Mar; 120(6):1036-47.JN

Abstract

To examine mechanisms underlying substance P (SP) release from primary sensory neurons in response to activation of the non-selective cation channel transient receptor potential ankyrin 1 (TRPA1), SP release from cultured rat dorsal root ganglion neurons was measured, using radioimmunoassay, by stimulating TRPA1 with allyl isothiocyanate (AITC), a TRPA1 agonist. AITC-evoked SP release occurred in a concentration- and time-dependent manner. Interestingly, p38 mitogen-activated protein kinase (p38) inhibitor SB203580 significantly attenuated AITC-evoked SP release. The in vivo effect of AITC-evoked SP release from primary sensory neurons in mice was evaluated. Hind paw intraplantar injection of AITC induced nociceptive behaviors and inflammation (edema, thermal hyperalgesia). AITC-induced thermal hyperalgesia and edema were inhibited by intraplantar pre-treatment with either SB203580 or neurokinin-1 receptor antagonist CP96345. Moreover, intrathecal pre-treatment with either CP96345 or SB203580 inhibited AITC-induced nociceptive behaviors and thermal hyperalgesia. Immunohistochemical studies demonstrated that intraplantar AITC injection induced the phosphorylation of p38 in mouse dorsal root ganglion neurons containing SP. These findings suggest that activation of TRPA1 evokes SP release from the primary sensory neurons through phosphorylation of p38, subsequent nociceptive behaviors and inflammatory responses. Furthermore, the data also indicate that blocking the effects of TRPA1 activation at the periphery leads to significant antinociception.

Authors+Show Affiliations

Department of Pharmacology, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan.No affiliation info availableNo 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

22182301

Citation

Nakamura, Yoki, et al. "Activation of Transient Receptor Potential Ankyrin 1 Evokes Nociception Through Substance P Release From Primary Sensory Neurons." Journal of Neurochemistry, vol. 120, no. 6, 2012, pp. 1036-47.
Nakamura Y, Une Y, Miyano K, et al. Activation of transient receptor potential ankyrin 1 evokes nociception through substance P release from primary sensory neurons. J Neurochem. 2012;120(6):1036-47.
Nakamura, Y., Une, Y., Miyano, K., Abe, H., Hisaoka, K., Morioka, N., & Nakata, Y. (2012). Activation of transient receptor potential ankyrin 1 evokes nociception through substance P release from primary sensory neurons. Journal of Neurochemistry, 120(6), 1036-47. https://doi.org/10.1111/j.1471-4159.2011.07628.x
Nakamura Y, et al. Activation of Transient Receptor Potential Ankyrin 1 Evokes Nociception Through Substance P Release From Primary Sensory Neurons. J Neurochem. 2012;120(6):1036-47. PubMed PMID: 22182301.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Activation of transient receptor potential ankyrin 1 evokes nociception through substance P release from primary sensory neurons. AU - Nakamura,Yoki, AU - Une,Yujiro, AU - Miyano,Kanako, AU - Abe,Hiromi, AU - Hisaoka,Kazue, AU - Morioka,Norimitsu, AU - Nakata,Yoshihiro, Y1 - 2012/02/06/ PY - 2011/12/21/entrez PY - 2011/12/21/pubmed PY - 2012/6/2/medline SP - 1036 EP - 47 JF - Journal of neurochemistry JO - J Neurochem VL - 120 IS - 6 N2 - To examine mechanisms underlying substance P (SP) release from primary sensory neurons in response to activation of the non-selective cation channel transient receptor potential ankyrin 1 (TRPA1), SP release from cultured rat dorsal root ganglion neurons was measured, using radioimmunoassay, by stimulating TRPA1 with allyl isothiocyanate (AITC), a TRPA1 agonist. AITC-evoked SP release occurred in a concentration- and time-dependent manner. Interestingly, p38 mitogen-activated protein kinase (p38) inhibitor SB203580 significantly attenuated AITC-evoked SP release. The in vivo effect of AITC-evoked SP release from primary sensory neurons in mice was evaluated. Hind paw intraplantar injection of AITC induced nociceptive behaviors and inflammation (edema, thermal hyperalgesia). AITC-induced thermal hyperalgesia and edema were inhibited by intraplantar pre-treatment with either SB203580 or neurokinin-1 receptor antagonist CP96345. Moreover, intrathecal pre-treatment with either CP96345 or SB203580 inhibited AITC-induced nociceptive behaviors and thermal hyperalgesia. Immunohistochemical studies demonstrated that intraplantar AITC injection induced the phosphorylation of p38 in mouse dorsal root ganglion neurons containing SP. These findings suggest that activation of TRPA1 evokes SP release from the primary sensory neurons through phosphorylation of p38, subsequent nociceptive behaviors and inflammatory responses. Furthermore, the data also indicate that blocking the effects of TRPA1 activation at the periphery leads to significant antinociception. SN - 1471-4159 UR - https://www.unboundmedicine.com/medline/citation/22182301/Activation_of_transient_receptor_potential_ankyrin_1_evokes_nociception_through_substance_P_release_from_primary_sensory_neurons_ L2 - https://doi.org/10.1111/j.1471-4159.2011.07628.x DB - PRIME DP - Unbound Medicine ER -