• Top page
  • Timetable
  • Per session
  • Per presentation
  • How to
  • Meeting Planner



Pain, Itch and Their Disorders

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

Alleviation of behavioral hypersensitivity in mouse models of inflammatory pain with two structurally different casein kinase 1 (CK1) inhibitors

  • P1-186
  • 栗原 崇 / Takashi Kurihara:1,2 櫻井 絵里 / Eri Sakurai:2 豊本 雅靖 / Masayasu Toyomoto:3 喜井 勲 / Isao Kii:3 川元 大輔 / Daisuke Kawamoto:1 朝田 俊秀 / Toshihide Asada:1 田邊 勉 / Tsutomu Tanabe:2 吉村 惠 / Megumu Yosimura:4 萩原 正敏 / Masatoshi Hagiwara:3 宮田 篤郎 / Atsuro Miyata:1 
  • 1:鹿児島大院・医・生体情報薬理 / Dept Pharmacol, Grad Sch Med and Dent Sci, Kagoshima Univ. 2:東京医歯大院・医・細胞薬理学 / Dept Pharmacol and Neurobiol, Grad Sch Med, Tokyo Med and Dent Univ 3:京都大学院・医・形態形成機構 / Dept Anat and Devel Biol, Grad Sch Med, Kyoto Univ 4:熊本保健科学大・院・保健科学 / Grad Sch Health Sci, Kumamoto Health Sci Univ 

The phylogenetically highly conserved CK1 protein kinases consisting of at least seven isoforms form a distinct family within the eukaryotic protein kinases. CK1 family members play crucial roles in a wide range of signaling activities. However, the functional role of CK1 in somatosensory pain signaling has not yet been fully understood. The aim of this study was to clarify the role of CK1 in the regulation of inflammatory pain in mouse carrageenan and complete Freund's adjuvant (CFA) models.
We have used two structurally different CK1 inhibitors, TG003 and IC261. TG003, which was originally identified as a cdc2-like kinase inhibitor, had potent inhibitory effects on CK1 isoforms in vitro and in cultured cells. Intrathecal injection of either TG003 (1-100 pmol) or IC261 (0.1-1 nmol) dose-dependently decreased mechanical allodynia and thermal hyperalgesia induced by carrageenan or CFA. Bath-application of either TG003 (1 μM) or IC261 (1 μM) had only marginal effects on spontaneous excitatory postsynaptic currents (sEPSCs) recorded in the substantia gelatinosa neurons of control mice. However, both compounds decreased the frequency of sEPSCs in both inflammatory pain models.
These results suggest that CK1 plays an important pathophysiological role in spinal inflammatory pain transmission, and that inhibition of the CK1 activity may provide a novel strategy for the treatment of inflammatory pain.

Copyright © Neuroscience2014. All Right Reserved.