Exploration and identification of novel therapeutic targets for dynamic tactile allodynia

我们发现，脊髓背角神经元的兴奋性增加，但不是初级传入，刷刺激参与动态触觉异常性疼痛的发展在带状疱疹相关疼痛的小鼠模型。为了鉴定在动态触觉异常性疼痛的发展中具有作用的候选基因，通过基因芯片寡核苷酸表达阵列分析脊髓的基因表达谱。在动态触觉异常性疼痛小鼠中上调的基因中，鉴定了P2X4受体、P2X7受体、S1P3受体和T淋巴细胞标记物。我们还发现，P2X4受体，P2X7受体，S1P3受体的表达增加和T淋巴细胞浸润的脊髓背角有助于动态触觉异常性疼痛的发展。这些结果表明，靶向P2X4受体，P2X7受体，S1P3受体和T淋巴细胞是治疗带状疱疹相关的动态触觉异常性疼痛的新的治疗策略。

We showed that increased excitability of spinal dorsal horn neurons, but not primary afferents, to brush stimulation is involved in the development of dynamic tactile allodynia in a murine model of herpes zoster-associated pain. To identify the candidate genes that have roles in the development of dynamic tactile allodynia, gene expression profiles of the spinal cord were analyzed by GeneChip oligonucleotide expression arrays. Among the genes upregulated in mice with dynamic tactile allodynia, P2X4 receptor, P2X7 receptor, S1P3 receptor and T-lymphocyte markers were identified. We also showed that increased expression of P2X4 receptor, P2X7 receptor, S1P3 receptor and T-lymphocyte infiltration in the spinal dorsal horn contribute to the development of dynamic tactile allodynia. These results suggest that targeting P2X4 receptor, P2X7 receptor, S1P3 receptor and T-lymphocytes is the new therapeutic strategy for treating herpes zoster-associated dynamic tactile allodynia.