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Possible involvement of TRPV1 and TRPV4 in nociceptive stimulation- induced nocifensive behavior and neuroendocrine response in mice.
Brain Res Bull. 2015 Sep; 118:7-16.BR

Abstract

Members of the transient receptor potential (TRP) family of ion channels play important roles in inflammation and pain. Here, we showed that both TRPV1 and TRPV4 might contribute to biphasic nocifensive behavior and neuroendocrine response following a formalin test. We subcutaneously injected saline, formalin, or the TRPV4 agonist, 4α-phorbol 12,13-didecanoate (4α-PDD) into one hindpaw of wild-type (WT), TRPV1-deficient (Trpv1(-/-)), and TRPV4-deficient (Trpv4(-/-)) mice to investigate nocifensive behaviors (phase I [0-10 min] and phase II [10-60 min]) and Fos expression in the dorsal horn of the spinal cord and other brain regions related to pain, in the paraventricular nucleus (PVN), paraventricular nucleus of the thalamus, the medial habenular nucleus, the medial nucleus of the amygdala and capsular part of the central amygdala. Subcutaneous (s.c.) injection of formalin caused less nocifensive behavior in Trpv1(-/-) and Trpv4(-/-) mice than in WT mice during phase I. In phase II, however, formalin induced less nocifensive behavior only in the Trpv1(-/-) mice, but not in the Trpv4(-/-) mice, relative to WT mice. The number of Fos-like immunoreactive (LI) neurons in laminae I-II of the dorsal horn increased in all types of mice 90 min after s.c. injection of formalin; however, there was no difference in the other regions between saline- and formalin-treated mice. Furthermore, s.c. injection of 4α-PDD did not induce nociceptive behavior nor influence the number of Fos-LI neurons in the all above mentioned regions in any of the mice. These results suggest that TRPV4-mediated nociceptive information from the peripheral tissue excluding the spinal pathway might be involved the formalin behavioral response during phase I. Only TRPV1 might regulate the formalin behavioral response in peripheral neuron.

Authors+Show Affiliations

Department of Physiology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan; Department of Orthopaedics, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan; Department of Orthopaedics, Youmeikai Obase Hospital, Kanda, Fukuoka 800-0344, Japan.Department of Orthopaedics, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.Department of Physiology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.Department of Physiology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.Department of Physiology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.Department of Physiology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan; Department of Orthopaedics, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.Department of Physiology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.Department of Physiology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.Department of Physiology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.Department of Orthopaedics, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.Department of Orthopaedics, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.Department of Orthopaedics, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.Department of Pharmacology, Jichi Medical University, Minamikawachi, Tochigi 329-0498, Japan.Edogawabashi Suzuki Clinic, Shinjyukuku, Tokyo 162-0801, Japan.Department of Physiology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan. Electronic address: yoichi@med.uoeh-u.ac.jp.

Pub Type(s)

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

Language

eng

PubMed ID

26314785

Citation

Ishikura, Toru, et al. "Possible Involvement of TRPV1 and TRPV4 in Nociceptive Stimulation- Induced Nocifensive Behavior and Neuroendocrine Response in Mice." Brain Research Bulletin, vol. 118, 2015, pp. 7-16.
Ishikura T, Suzuki H, Shoguchi K, et al. Possible involvement of TRPV1 and TRPV4 in nociceptive stimulation- induced nocifensive behavior and neuroendocrine response in mice. Brain Res Bull. 2015;118:7-16.
Ishikura, T., Suzuki, H., Shoguchi, K., Koreeda, Y., Aritomi, T., Matsuura, T., Yoshimura, M., Ohkubo, J., Maruyama, T., Kawasaki, M., Ohnishi, H., Sakai, A., Mizuno, A., Suzuki, M., & Ueta, Y. (2015). Possible involvement of TRPV1 and TRPV4 in nociceptive stimulation- induced nocifensive behavior and neuroendocrine response in mice. Brain Research Bulletin, 118, 7-16. https://doi.org/10.1016/j.brainresbull.2015.08.004
Ishikura T, et al. Possible Involvement of TRPV1 and TRPV4 in Nociceptive Stimulation- Induced Nocifensive Behavior and Neuroendocrine Response in Mice. Brain Res Bull. 2015;118:7-16. PubMed PMID: 26314785.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Possible involvement of TRPV1 and TRPV4 in nociceptive stimulation- induced nocifensive behavior and neuroendocrine response in mice. AU - Ishikura,Toru, AU - Suzuki,Hitoshi, AU - Shoguchi,Kanako, AU - Koreeda,Yuki, AU - Aritomi,Takafumi, AU - Matsuura,Takanori, AU - Yoshimura,Mitsuhiro, AU - Ohkubo,Jun-ichi, AU - Maruyama,Takashi, AU - Kawasaki,Makoto, AU - Ohnishi,Hideo, AU - Sakai,Akinori, AU - Mizuno,Atsuko, AU - Suzuki,Makoto, AU - Ueta,Yoichi, Y1 - 2015/08/24/ PY - 2015/03/10/received PY - 2015/07/30/revised PY - 2015/08/19/accepted PY - 2015/8/29/entrez PY - 2015/9/1/pubmed PY - 2016/8/23/medline KW - Formalin test KW - Neuroendocrine response KW - Nocifensive behavior KW - TRPV1 KW - TRPV4 SP - 7 EP - 16 JF - Brain research bulletin JO - Brain Res Bull VL - 118 N2 - Members of the transient receptor potential (TRP) family of ion channels play important roles in inflammation and pain. Here, we showed that both TRPV1 and TRPV4 might contribute to biphasic nocifensive behavior and neuroendocrine response following a formalin test. We subcutaneously injected saline, formalin, or the TRPV4 agonist, 4α-phorbol 12,13-didecanoate (4α-PDD) into one hindpaw of wild-type (WT), TRPV1-deficient (Trpv1(-/-)), and TRPV4-deficient (Trpv4(-/-)) mice to investigate nocifensive behaviors (phase I [0-10 min] and phase II [10-60 min]) and Fos expression in the dorsal horn of the spinal cord and other brain regions related to pain, in the paraventricular nucleus (PVN), paraventricular nucleus of the thalamus, the medial habenular nucleus, the medial nucleus of the amygdala and capsular part of the central amygdala. Subcutaneous (s.c.) injection of formalin caused less nocifensive behavior in Trpv1(-/-) and Trpv4(-/-) mice than in WT mice during phase I. In phase II, however, formalin induced less nocifensive behavior only in the Trpv1(-/-) mice, but not in the Trpv4(-/-) mice, relative to WT mice. The number of Fos-like immunoreactive (LI) neurons in laminae I-II of the dorsal horn increased in all types of mice 90 min after s.c. injection of formalin; however, there was no difference in the other regions between saline- and formalin-treated mice. Furthermore, s.c. injection of 4α-PDD did not induce nociceptive behavior nor influence the number of Fos-LI neurons in the all above mentioned regions in any of the mice. These results suggest that TRPV4-mediated nociceptive information from the peripheral tissue excluding the spinal pathway might be involved the formalin behavioral response during phase I. Only TRPV1 might regulate the formalin behavioral response in peripheral neuron. SN - 1873-2747 UR - https://www.unboundmedicine.com/medline/citation/26314785/Possible_involvement_of_TRPV1_and_TRPV4_in_nociceptive_stimulation__induced_nocifensive_behavior_and_neuroendocrine_response_in_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0361-9230(15)30023-X DB - PRIME DP - Unbound Medicine ER -