論文

査読有り 国際誌
2018年1月1日

Peripheral nerve injury-induced rearrangement of neural circuit in the spinal dorsal horn revealed by cross-correlation analysis.

Neuroscience letters
  • Yu Takemura
  • ,
  • Shunsaku Kobayashi
  • ,
  • Eiko Kato
  • ,
  • Shigeki Yamaguchi
  • ,
  • Yuuichi Hori

662
開始ページ
259
終了ページ
263
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.neulet.2017.10.044

Peripheral nerve injury often induces abnormal pain states, such as hyperalgesia and allodynia. In this study, we attempted to elucidate how neurons are synaptically integrated into the neuronal circuitry in the spinal dorsal horn and how synaptic connectivity patterns among dorsal horn neurons are altered by peripheral nerve injury. Experiments were performed on 6-8-week-old ICR mice. Partial sciatic nerve ligation was performed. Transverse slices of the lumbar spinal cord were prepared. Spike activities were simultaneously recorded from multiple neurons in the superficial dorsal horn (SDH) using a multi-electrode array system, and cross-correlograms between spike trains of neuron pairs were constructed. In sham-operated control mice, except for the flat cross-correlogram, the most common pattern was a cross-correlogram suggestive of common excitatory synaptic inputs to neuronal pairs. Peripheral nerve ligation increased the incidences of cross-correlograms suggestive of common excitatory synaptic inputs and excitatory synaptic connections, and decreased that of inhibitory synaptic connections. Additionally, bath-applied capsaicin, an agonist for transient receptor potential vanilloid 1 receptor, increased the frequency of action potentials. The effects of capsaicin stimulation on the incidence of cross-correlograms with various patterns were significantly different between sham-operated control and sciatic nerve-ligated mice. The present observations seem to indicate that neurons in the SDH form excitatory and/or inhibitory synapses with nearby neurons, and that synaptic connections among neurons in the SDH may remarkably change after the development of neuropathic pain.

リンク情報
DOI
https://doi.org/10.1016/j.neulet.2017.10.044
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/29079432
ID情報
  • DOI : 10.1016/j.neulet.2017.10.044
  • PubMed ID : 29079432

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