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Pain, Itch and Their Disorders

開催日 2014/9/11
時間 16:00 - 17:00
会場 Poster / Exhibition(Event Hall B)

The axonal transport and analgesic effect of newly developed Botulinum neurotoxin type A

  • P1-184
  • 丸濵 功太郎 / Kotaro Maruhama:1 松香 芳三 / Yoshizo Matsuka:2 山本 由弥子 / Yumiko Yamamoto:3 寺山 隆司 / Ryuji Terayama:1 杉本 朋貞 / Tomosada Sugimoto:1 
  • 1:岡山大院医歯薬口腔機能解剖 / Dept of Oral Function and Anatomy, Grad Sch of Med, Dent and Pharm Sci, Okayama Univ, Okayama, Japan 2:徳島大院ヘルスバイオサイエンス顎機能咬合再建 / Dept Stomatognathic Function and Occlusal Reconstruction, Tokushima Univ, Tokushima, Japan 3:岡山大院医歯薬病原細菌 / Dept of Bacteriology, Grad Sch of Med, Dent and Pharm Sci, Okayama Univ, Okayama, Japan 

The antigenicity of commercially available botulinum toxin (Botox) has been a dose-limiting factor for its clinical use. The antigenicity can be reduced by the removal of non-toxic component (BoNT/A). Here we demonstrate that BoNT/A is endocytosed and axonally transported by the trigeminal ganglion (TG) neurons and attenuates the magnitude of pain-related behaivior in a rat model of neuropathic pain. The analgesic effect of BoNT/A was evaluated by subcutaneously injecting the neurotoxin into the vibrissal pad of rats with a chronic constriction injury of the infraorbital nerve. Thermal testing was based on Neubert et al. (Pain. 2005). Fasted rat's desire to obtain a food reward was coupled to its ability to tolerate facial contact with a warm (45 °C) thermode. The neuropathy decreased the ratio of thermode contact duration / event. One week after the injury subcutaneous BoNT/A reduced the incidence of facial contacts and increased the duration / event indicating decreased thermal hyperalgesia. To confirm the axonal transport of subcutaneously administered BoNT/A, BoNT/A heavy chain (membrane binding subunit of BoNT/A) was labeled with Thiol-Reactive Probes and injected into the facial skin. Two hours later BoNT/A was detected in TG neurons. This label was inhibited by colchicine treatment. In conclusion, subcutaneous BoNT/A was axonally transported by TG neurons and reduced neuropathy symptoms.

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