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Plastic changes in the spinal cord and chronic pain Megumu Yoshimura 1 , Hidemasa Furue 1 , Terumasa Nakatsuka 1 , Akitoshi Itoh 1 , Toshihiko Katafuchi 1 1Department of Integrative Physiology, Graduate School of Medical Scienes, Kyushu University Keyword: 可塑性 , 慢性疼痛 , 軸索発芽 , 神経栄養因子 pp.935-940
Published Date 2004/12/10
DOI https://doi.org/10.11477/mf.1431100255
  • Abstract
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 Mechanisms for chronic pain induced by peripheral injury or inflammation have been extensively explored, and demonstrated that those are not only due to sensory receptor sensitizations but also due to plastic changes in the central nervous system. Following inflammation, several chemical mediators, including prostaglandin, and neurotrophic factor such as BDNF are released in the spinal cord which are thought to play an critical role in the induction of plasticity. In the present study, we investigated a plastic change following inflammation in the spinal dorsal horn by means of in vitro and in vivo patch-clamp recordings from substantia gelatinosa(SG, laminaⅡof Rexed)neurons. In normal condition, SG neurons received inputs preferentially from Aδafferents and/or C afferent fibers and Aβafferent inputs were detected in only 2%of neurons. On the other hand, in the early phase of inflammation(2 to 3 days after inflammation), substantial number of SG neurons received polysynaptic inputs from Aβafferents which originally terminated at the deep dorsal horn, and subsequently those afferents sprouted into SG and made monosynaptic contacts with SG neurons 5 to 7 days after inflammation. It is conceivable that the plastic changes in the sensory circuitry observed in the inflamed rats were a part of regeneration processes. Therefore, we next tested whether the circuitry following inflammation had a similarity with that of the neonatal rat spinal cord. Monosynaptic inputs from primary afferent to SG neurons in neonatal rats spinal cord(3 week old)were largely from Aβafferents and a small population of neurons had monosynaptic inputs from Aδafferents. Direct inputs from C afferents were detected in a few neurons. Thus, the synaptic circuitry in the neonatal rat spinal cord is similar to those of inflamed rats, with the exception of low incidence of C afferent inputs. These observations suggest that the sprouting of Aβafferents to SG neurons is a part of the regenerative process. However, the processes observed in the inflamed rats would not be exactly the same as those of development, such different might be the underlying mechanisms for hyperalgesia in inflamed condition. Therefore, clarification of the differences between the processes of development and reorganization of the synaptic circuitry following the inflammation should be the one of essential steps for understanding the pathological pain and might provide a therapeutic target.


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電子版ISSN 1882-1243 印刷版ISSN 0001-8724 医学書院

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