In the axotomized facial nucleus (axotFN), the levels of choline acetyltransferase, vesicular acetylcholine transporter, and gamma amino butyric acid A receptor α1 are decreased, after which the microglia begin to proliferate around injured motoneuron cell bodies. We conjectured that an injury signal released from the injured motoneurons triggers the microglial proliferation in the axotFN. However, it is unclear whether the level of microglial proliferation is dependent on the degree of motoneuronal insult. In this study, we investigated the relationship between the extents of motoneuronal injury and microglial proliferation in a rat axotFN model. Administration of glial cell line-derived neurotrophic factor, N-acetyl L-cysteine, or salubrinal at the transection site ameliorated the increase in c-Jun and the reductions in levels of phosphorylated cAMP response element binding protein (p-CREB) and functional molecules in the injured motoneurons. Concurrently, the levels of the microglial marker ionized calcium-binding adapter molecule 1 and of macrophage colony-stimulating factor (cFms), proliferating cell nuclear antigen, and p-p38/p38 were significantly downregulated in microglia. These results demonstrate that the recovery of motoneuron function resulted in the reduction in microglial proliferation. We conclude that the degree of neuronal injury regulates the levels of microglial proliferation in the axotFN.

中文翻译：

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受损运动神经元的恢复减少了成年大鼠面核中的小胶质细胞增殖

在轴突面核（axotFN）中，胆碱乙酰转移酶、囊泡乙酰胆碱转运蛋白和γ氨基丁酸A受体α1的水平降低，之后小胶质细胞开始在受损的运动神经元细胞体周围增殖。我们推测受伤的运动神经元释放的损伤信号触发了 axotFN 中的小胶质细胞增殖。然而，目前尚不清楚小胶质细胞增殖的水平是否取决于运动神经元损伤的程度。在本研究中，我们研究了大鼠 axotFN 模型中运动神经元损伤程度与小胶质细胞增殖之间的关系。在横断部位施用神经胶质细胞系源性神经营养因子、N-乙酰基 L-半胱氨酸或 salubrinal 可改善 c-Jun 的增加以及磷酸化 cAMP 反应元件结合蛋白 (p-CREB) 和功能分子水平的降低在受伤的运动神经元中。同时，小胶质细胞中小胶质细胞标记物离子化钙结合接头分子 1 和巨噬细胞集落刺激因子 (cFms)、增殖细胞核抗原和 p-p38/p38 的水平显着下调。这些结果表明运动神经元功能的恢复导致小胶质细胞增殖的减少。我们得出的结论是，神经元损伤的程度调节 axotFN 中小胶质细胞的增殖水平。