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



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)

Astrocyte induce cortical synapse remodeling in neuropathic pain model mice

  • S3-F-3-3
  • 鍋倉 淳一 / Junichi Nabekura:1 金 善行 / Kwang Sun KIm:2 小泉 修一 / Schuichi Koizumi :2,3 
  • 1:自然科学研究機構 生理学研究所 / National Institute for Physiological Sciences, Japan 2:科学技術振興機構 / JST, Japan 3:山梨大学 / Dept. Pharmacol., Facult. Med,Univ. Yamanashi, Yamanashi, Japan 

Peripheral nerve injury/tissue inflammation triggers maladaptive plastic changes along the somatosensory system so that altered nociceptive signal processing, represented by tactile allodynia occurs. It is suggested that early afferent barrage can drive subsequent alterations in the central nervous system, including the cortex, that in turn contribute to neuropathic/chronic pain. Recent advance in imaging techniques, e.g. functional MRI and PET, allows us to understand the activation of various higher brain areas in case of chronic pain. However, due to the spatial limitation of these approaches, it is difficult to directly observe plastic change of more fine structures, e.g. neurons and synapses in vivo. Two photon excitation of fluorescent molecules enables us to observe the fine structures and neuronal activity in the various organs and tissues in an in vivo condition. Here, we introduce plastic changes of dynamics of neuronal structures and activities n the brain of living chronic pain mice. Spine turnover in the primary somatosensory cortex corresponding to the injured paw markedly increased during an early phase of neuropathic pain and was restored in a late phase of neuropathic pain. New spines that generated before nerve injury showed volume decrease after injury, whereas more new spines that formed in the early phase of neuropathic pain became persistent and substantially increased their volume during the late phase. Further, preexisting stable spines survived less following injury than controls, and such lost persistent spines were smaller in size than the surviving ones, which displayed long-term potentiation-like enlargement over weeks. Thus, peripheral nerve injury induces rapid and selective remodeling of cortical synapses, which is associated with neuropathic pain development. Indeed, spontaneous activity of layer 2/3 neurons in the primary somatosensory cortex in vivo increased under chronic pain. Thus, the synaptic remodeling of somatosensory cortex leads to the exaggerated neuronal response in the somatosensory cortex e.g. an increases of neurons responded in number and response probability, which could be the underlying mechanism in the allodynia.

Copyright © Neuroscience2014. All Right Reserved.