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Pain, Itch and Their Disorders

開催日 2014/9/11
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

Role of CGRP in inflammatory pain-induced potentiation in the central amygdala

  • P1-191
  • 篠原 恵 / Kei Shinohara:1,2,3 池田 亮 / Ryo Ikeda:1 高橋 由香里 / Yukari Takahasi:2,3 栗原 裕基 / Hiroki Kurihara:4 丸毛 啓史 / Keishi Marumo:1 加藤 総夫 / Fusao Kato:2,3 
  • 1:慈恵医大・整形外科 / Dept. Orthop., Jikei Univ. Sch. Med., Tokyo, Japan 2:慈恵医大・神経科学研究部 / Dept. Neurosci., Jikei Univ. Sch. Med., Tokyo, Japan 3:慈恵医大・痛み脳科学センター / Center for Neuroscience of Pain, Jikei Univ. Sch. Med., Tokyo, Japan 4:東京大院・代謝生理化学 / Dept. Mol. Cell Biol., Grad. Sch. Med., Univ. of Tokyo, Tokyo, Japan 

Nociceptive signals arising from the periphery carry sensory information that help the amygdala form negative emotion of pain (Neugebauer et al., 2003; Ikeda et al., 2007; Veinante et al., 2013). Of various routes sending such information, the spino-parabrachio-amygdaloid pathway is most essential because it directly conveys nociceptive information from the spinal cord to the central amygdala without intermediary of thalamo-cortical pathways. Interestingly, calcitonin gene-related peptide (CGRP), a mediator well known to underlie peripheral inflammatory responses (Hirsch et al, 2013), is also expressed in the final step projections of this pathway, i.e., those from the lateral parabrachial nucleus (LPB) to the capsular division of the central amygdala (CeC; Han et al., 2005; Dong et al., 2010). Indeed, CGRP receptor antagonists attenuate the arthritis-induced potentiation of the LPB-CeC synaptic transmission (Han et al., 2005). However, it remains undetermined whether release of CGRP is essential in establishing LPB-CeC potentiation after inflammatory pain. We examined this possibility by analyzing LPB-CeC transmission in the inflammatory pain model created in the mice deficient of CGRP (CGRP-/-; Oh-hashi et al., 2001). Whereas the CGRP-/- mice showed significant decrease in nocifensive behaviors for only a brief period (20-25 min) following intraplantar formalin injection in the left, the amplitude of the evoked excitatory postsynaptic currents (EPSCs; evoked by 600-1000 μA stimulation of LPB pathways), as recorded from the CeC in slices prepared at 6 hrs post-injection, was significantly larger in the right CeC from wild type mice than that from the CGRP-/- mice and from the mice receiving intraplantar saline injection. It is thus likely that, in addition to its well described role in the peripheral inflammation, CGRP in the LPB-CeC pathway might underlie delayed-onset potentiation of the central link between nociception and emotion in the course of pain chronification and would be an important target for therapies to prevent development of chronic pain.

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