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Pain Brain

開催日 2014/9/13
時間 17:10 - 19:10
会場 Room F(302)
Chairperson(s) 富永 真琴 / Makoto Tominaga (自然科学研究機構 岡崎統合バイオサイエンスセンター(生理学研究所)細胞生理研究部門 / Division of Cell Signaling, Okazaki Institute for Integrative Bioscience (National Institute for Physiological Sciences), National Inst)

Amygdala plasticity in the chronification process of inflammatory pain

  • S3-F-3-1
  • 加藤 總夫 / Fusao Kato:1,2 
  • 1:東京慈恵会医科大学・神経科学研究部 / Dept Neurosci, Jikei Univ Sch Med, Japan 2:東京慈恵会医科大学・痛み脳科学センター / Center for Neuroscience of Pain, Jikei Univ Sch Med, Japan 

The central amygdala (CeA) plays pivotal roles in the link between nociception and emotion (Veinante et al, 2013). Because the CeA receives di-synaptic projection from the peripheral C fibers via the superficial layer of the dorsal horn and the lateral parabrachial nucleus (LPB), it is likely that C fiber-mediated information would play substantial roles in activating this pathway and promoting synaptic plasticity in the LPB-CeA synaptic transmission. Indeed, an ablation of peripheral C fibers with neonatal capsaicin treatment prevents LPB-CeA potentiation in the rats with spinal nerve ligation-induced neuropathy showing potent mechanical allodynia (Nakao et al, 2012). In a recent series of experiments, we analyzed consequences of inflammatory pain caused by subcutaneous formalin injection at >6-hours post-injection long after the primary acute nociceptive phases. 1) LPB-CeA potentiation, as confirmed by excitatory postsynaptic current recordings in acute slices prepared 6 hours after intraplantar formalin injection, was markedly attenuated in mice lacking CGRP protein (provided by H. Kurihara, University of Tokyo Graduate School). 2) Subcutaneous formalin injection into the perioral skin resulted in robust LPB-CeA potentiation at 6 hours post-injection, only in the right CeA. 3) This also resulted in modified patterns of the spontaneous choice of floors with distinct near-noxious temperatures. It is suggested that the persistent inflammatory activation following the primary acute nociception would be the key signal for the nociception-triggered amygdala plasticity, regardless of the site of inflammation, to affect aversive sensation-dependent behaviors. Collaborations with Shinohara K, Sugimoto M, Miyazawa Y, Sugimura Y, Takahashi Y and Watabe AM are acknowledged.

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