Following the transection of peripheral sympathetic preganglionic axons comprising the cervical sympathetic trunk (CST), we observe robust glial and neuronal plasticity at 1 week post-injury in the rat spinal cord intermediolateral cell column (IML), which houses the injured parent neuronal cell bodies. This plasticity contributes to neuroprotection, as no neuronal loss in the IML is present at 16 weeks post-injury. Here, we administered the antibiotic minocycline or vehicle (VEH) daily for 1 week after CST transection to investigate the role of activated microglia in IML glial and neuronal plasticity and subsequent neuronal survival. At 1 week post-injury, minocycline treatment did not alter microglia number in the IML, but led to a dampened microglia activation state. In addition, the increases in oligodendrocyte (OL) lineage cells and activated astrocytes following injury in VEH rats were attenuated in the minocycline-treated rats. Further, the normal downregulation of choline acetyltransferase (ChAT) in the injured neurons was blunted. At 16 weeks post-injury, fewer ChAT+ neurons were present in the minocycline-treated rats, suggesting that activated microglia together with the glial and neuronal plasticity at 1 week post-injury contribute to the long-term survival of the injured neurons. These results provide evidence for beneficial crosstalk between activated microglia and neurons as well as other glial cells in the cord following peripheral axon injury, which ultimately leads to neuroprotection. The influences of microglia activation in promoting neuronal survival should be considered when developing therapies to administer minocycline for the treatment of neurological pathologies.

中文翻译：

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周围轴突损伤后大鼠脊髓中激活的小胶质细胞促进神经胶质和神经元可塑性，这对于长期神经元生存是必要的。


在横断包含颈交感干（CST）的外周交感神经节前轴突后，我们在损伤后1周的大鼠脊髓中间外侧细胞柱（IML）中观察到强大的神经胶质和神经元可塑性，该细胞柱容纳受伤的亲代神经元细胞体。这种可塑性有助于神经保护，因为损伤后 16 周 IML 中不存在神经元损失。在这里，我们在 CST 横断后每天给予抗生素米诺环素或载体 (VEH) 1 周，以研究活化的小胶质细胞在 IML 胶质和神经元可塑性以及随后的神经元存活中的作用。损伤后 1 周，米诺环素治疗没有改变 IML 中的小胶质细胞数量，但导致小胶质细胞激活状态减弱。此外，VEH 大鼠损伤后少突胶质细胞 (OL) 谱系细胞和活化星形胶质细胞的增加在米诺环素治疗的大鼠中减弱。此外，受损神经元中胆碱乙酰转移酶（ChAT）的正常下调被削弱。损伤后 16 周，米诺环素治疗的大鼠中存在较少的 ChAT+ 神经元，这表明损伤后 1 周激活的小胶质细胞以及神经胶质和神经元可塑性有助于受损神经元的长期存活。这些结果为周围轴突损伤后激活的小胶质细胞和神经元以及脊髓中其他神经胶质细胞之间的有益串扰提供了证据，最终导致神经保护。在开发米诺环素治疗神经病理学的疗法时，应考虑小胶质细胞激活对促进神经元存活的影响。