Mechanism of pain generation in the rat model of brachial plexus avulsion and the effect of anti-nerve growth factor receptor (p75 neurotrophin receptor) administration

臂丛神经撕脱大鼠模型疼痛产生机制及抗神经生长因子受体（p75神经营养素受体）给药的影响

• 批准号: 23592158
• 负责人: KUNIYOSHI Kazuki
• 金额: $ 2.33万
• 依托单位: Chiba University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2013
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23592158/
• 关键词: 腕神経叢損傷; 疼痛; 機序; p75NTR阻害; microglia; astrocyte; satellite cell

In the rat model of brachial plexus avulsion (BPA), pain-related behavior and the extent of glial activation was evaluated. The effect of local and general administration of anti-nerve growth factor receptor (p75 neurotrophin receptor [p75NTR]) antibodies was also evaluated in the BPA model. As a result, rats in the BPA group displayed significant mechanical hyperalgesia in the dermatome innervated by uninjured nerves both ipsilaterally and contra laterally. GFAP-immunoreactive astrocytes and Iba1-immunoreactive microglia were significantly activated on the ipsilateral side in the BPA group. And in the both rats group in which anti-p75NTR was locally or generally, mechanical hyperalgesia was significantly improved. Levels of GFAP-immunoreactive astrocytes and Iba1-immunoreactive microglia in the anti-p75NTR group were significantly reduced.

在臂丛神经撕脱（BPA）的大鼠模型中，疼痛相关的行为和神经胶质激活的程度进行了评价。还在BPA模型中评价了局部和全身给予抗神经生长因子受体（p75神经营养因子受体[p75NTR]）抗体的作用。结果，BPA组大鼠在同侧和对侧未损伤神经支配的皮节中显示出显著的机械性痛觉过敏。BPA组同侧GFAP免疫反应阳性星形胶质细胞和Iba1免疫反应阳性小胶质细胞明显活化。局部或全身应用抗p75NTR的两组大鼠机械性痛觉过敏均得到明显改善。抗p75 NTR组GFAP免疫反应阳性星形胶质细胞和Iba1免疫反应阳性小胶质细胞的水平显著降低。