<b>Biochemical and physical treatment in rat neuropathic </b><b>pain and nerve growth factor </b>

• Nishi Mitsuharu

  Department of Laboratory Sciences, Yamaguchi University School of Medicine Medical Appliance Co. Ltd.

• Ishikawa Toshizo

  Department of Laboratory Sciences, Yamaguchi University School of Medicine

• Matsumoto Yoshihiro

  Department of Laboratory Sciences, Yamaguchi University School of Medicine Department of Dental Anesthesiology, Kyusyu Dental College

• Katsube Nobuo

  Minase Res. Inst., Ono Pharmaceutical Co., Ltd.

• Tateishi Naruto

  Minase Res. Inst., Ono Pharmaceutical Co., Ltd.

• Yonamine Haruno

  Department of Laboratory Sciences, Yamaguchi University School of Medicine

• Matsui Tomohiro

  Department of Laboratory Sciences, Yamaguchi University School of Medicine

• Okano Kozue

  Department of Laboratory Sciences, Yamaguchi University School of Medicine

• Suzuki Hidenori

  Department of Laboratory Sciences, Yamaguchi University School of Medicine Department of Orthopedic Surgeries, Yamaguchi University, School of Medicine

• Kataoka Hideo

  Department of Laboratory Sciences, Yamaguchi University School of Medicine Department of Orthopedic Surgeries, Yamaguchi University, School of Medicine

• Nakanishi Osamu

  Department of Dental Anesthesiology, Kyusyu Dental College

Bibliographic Information

Other Title

• <b>神経因性疼痛に対する物理学的および神経化学的治療法と神経成長因子 </b>

Abstract

   The mechanisms of neuropathic pain following peripheral nerve injury have not been fully understood. Although it has recently reported that nerve growth factor (NGF) is possibly involved in regeneration of injured peripheral sensory neurons, there are only few evidences to confirm it in neuropathic pain. Therefore, we characterized the role of NGF in neuropathic pain after nerve injury by different action of treatments.<br>   Sprague-Dawley rats were subjected and the left sciatic nerve was loosely ligated (CCI model). To quantify the pain sensation the paw withdrawal latency (PWL) against thermal stimulation was periodically measured after CCI. Either day 5 or 14, the rats were subjected for microdialysis and perfused fixation for immunohistochemistry (c-fos). The modulatory effect of anti-NGF either with N-type Ca²⁺ channels blocker (ONO-2921) or magnetic field stimulation (MF) was considered.<br>   The PWL were increased with time from day 3 to day 14 after CCI. On day 5 to 14, the c-fos positive cells at Rexed 1-2 and 5-6 were seen accompanied with slight damage of Rexed 3-4 neurons (HE). 4-methyl catechol, as an inducer of NGF, attenuated neuropathic pain and this effect was moderately antagonized by anti-NGF. These behavioral and cell functional changes were significantly attenuated by ONO-2921 or MF treatments. However, the attenuating effect of MF was antagonized by anti-NGF while effects of ONO-2921 did not affect any.<br>   It is concluded that the neuropathic pain may result in excessive spinal glutamate release followed by an early gene expression at input region of c-fiber as “neuronal plasticity”. Further more, we suggest that insufficient of NGF may possibly be developing neuropathic pain and that magnetic field stimulation has beneficial effect through mechanisms by acceleration of neuronal regeneration induced by NGF. However, beneficial effect of N-type Ca²⁺ channels blocker may not involved by synthesis of NGF.

Journal

• PAIN RESEARCH

  PAIN RESEARCH 19 (4), 141-149, 2004

  JAPANESE ASSOCIATION FOR STUDY OF PAIN

Keywords

• neuropathic pain
• neuroplasticity
• CSf-glutamate
• c-fos expression
• magnetic field stimulation
• N-type Ca²⁺ channel blocker

Details

• CRID: 1390001204367008128
• NII Article ID: 130004651862
• NII Article ID: 10013596382
• NII Book ID: AN10195934
• DOI: 10.11154/pain.19.141
• ISSN: 21874697
• ISSN: 09158588
• Web Site: https://www.jstage.jst.go.jp/article/pain/19/4/19_3/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2006193332
• Text Lang: ja
• Data Source:
  • JaLC
  • Crossref
  • CiNii Articles
• Abstract License Flag: Disallowed