Interaction between dorsal horn neuron subsets operated by a neuropeptide Y and prodynorphin promoter and its contribution to Aβ fiber–induced allodynia–like behavior in rats

DOI Web Site 参考文献13件 オープンアクセス
  • Sueto Daichi
    Department of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University
  • Ishibashi Tadayuki
    Department of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University Department of Anesthesiology and Critical Care Medicine, Graduate School of Medical Sciences, Kyushu University
  • I Eriko
    Department of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University
  • Tashima Ryoichi
    Department of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University
  • Yoshikawa Yu
    Department of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University
  • Yamaura Ken
    Department of Anesthesiology and Critical Care Medicine, Graduate School of Medical Sciences, Kyushu University
  • Tsuda Makoto
    Department of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University Kyushu University Institute for Advanced Study

説明

<p>Allodynia, pain induced by innocuous mechanical stimuli, is attributed to central nervous system dysfunction. We recently identified spinal dorsal horn (SDH) neuronal subsets that were captured by adeno–associated virus (AAV) vectors carrying a promoter of neuropeptide Y or prodynorphin (AAV–NpyP and –PdynP, respectively). Our previous studies demonstrated that both AAV–NpyP+ neuron inhibition and AAV–PdynP+ neuron excitation contribute to neuropathic allodynia–like behavior in rats. However, the potential interaction between these two subsets remains unknown. The present study employed tools that enable the optogenetic stimulation of touch–sensing Aβ fibers and neuronal subset–selective manipulations. Our findings revealed that the Aβ fiber–derived allodynia–like behavior in rats with AAV–NpyP+ neuron ablation was prevented by the simultaneous ablation of AAV–PdynP+ neurons. Furthermore, the removal of AAV–NpyP+ neurons allowed AAV–PdynP+ neurons to receive Aβ fiber–derived excitatory inputs. These results reveal an interaction between these subsets that are crucial for Aβ fiber–mediated allodynia.</p>

収録刊行物

  • PAIN RESEARCH

    PAIN RESEARCH 39 (1), 40-45, 2024-05-13

    一般社団法人 日本疼痛学会

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