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Ion Channels and Excitable Membranes

開催日 2014/9/12
時間 14:00 - 15:00
会場 Poster / Exhibition(Event Hall B)

Carrageenan-induced iflammation increase Cav3.2 expression within distinct subgroups of mouse DRG neurons

  • P2-006
  • 渡辺 正哉 / Masaya Watanabe:1 植田 高史 / Takashi Ueda:1 柴田 泰宏Yasuhiro Shibata 星川 真理子Mariko Hoshikawa 熊本 奈都子 / Natsuko Kumamoto:1 鵜川 眞也 / shinya Ugawa:1 
  • 1:名古屋市立大学 / Dept. of Neurobiol. and Anat., Grad. Sch. of Med. Sci., Nagoya City University 

Carrageenan-induced inflammation increased Cav3.2 expression within distinct subgroups of mouse DRG neurons.

Masaya Watanabe, Takashi Ueda, Yasuhiro Shibata, Mariko Hoshikawa, Nastuko Kumamoto, Shinya Ugawa
Dept. of Neurobiol. and Anat., Grad. Sch. of Med. Sci., Nagoya City Univ., Nagoya, Japan

T-type calcium channels encoded by the Cav3.2 isoform are expressed in primary sensory neurons of dorsal root ganglion (DRG). In rats, they contribute to nociceptive pain and pathological pains referred to as allodynia and hyperalgesia. However, the expression patterns of Cav3.2 channels in rat DRG neurons (Rose et al., 2013) were quite different from those in mice reported by Shin et al. (2003). Thus, it is still unknown whether Cav3.2 play an important role in hyperalgesia induced by inflammatory agents in mice. In the present study, we made an experimental model of inflammatory pain induced by injection of carrageenan into the mouse hindpaw, assessed mechanical hyperalgesia by Von Frey test, and performed quantitative RT-PCR and Western blot analyses, and double immunofluorescence staining for Cav3.2 in combination with DRG neuronal markers (peripherin, IB4, NF-H, CGRP and TRPV1) in the L5 DRG. As reported before, unilateral carrageenan injections caused mechanical hyperalgesia on the ipsilateral side in the mice. Cav3.2 was upregulated at day 2 (sub-acute phase) at mRNA and protein levels, suggesting that involvement of Cav3.2 in the sub-acute phase of inflammatory hyperalgesia. Interestingly, immunohistochemical analysis revealed that carrageenan injection increased the percentage of Cav3.2-positive neurons within the L5 DRG on the ipsilateral sides at day 2. Moreover, the inflammation-induced increase in Cav3.2-positive neurons was significantly observed in TRPV1-immunoreactive neurons. Finally, intraplantar treatment with mibefradil and NNC 55-0396, T-type calcium channel blockers significantly improved the primary mechanical hyperalgesia. These data suggest that Cav3.2 participates in the development of inflammatory hyperalgesia and play an ever-greater role in sub-acute phase of inflammatory pains by co-localizing with TRPV1 receptors in mice.

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