Politis M J, Miller J E
Brain Res. 1985 Dec 16;359(1-2):183-6. doi: 10.1016/0006-8993(85)91427-1.
Glutamine synthetase (GS) was assessed distal to the site of axonal injury in traumatized rat central (optic) or peripheral (tibial) nerve prior to and during periods of reactive PNS and CNS glial cell hypertrophy. GS activity in crushed optic nerve remained equivalent to that in unoperated control tissue at 2 days postoperatively, but rose by 30% at 7 and 12 days after surgery. In contrast, GS activity in traumatized peripheral nerve was significantly lower than in unoperated controls at 7 and 12 days postoperatively. Administration of mitotic inhibitor (AraC, cytosine arabinofuranoside) prevented significant trauma-induced alterations in GS activity in optic nerves at 7, and in peripheral nerves at 7 and 12 days postoperatively. Results suggest significant alterations in glial/Schwann GS activity after nerve fiber injury and that these alterations can be delayed/prevented by administration of mitotic inhibitors.
在反应性周围神经系统（PNS）和中枢神经系统（CNS）神经胶质细胞肥大之前及期间，对遭受创伤的大鼠中枢（视神经）或外周（胫神经）神经轴突损伤部位远端的谷氨酰胺合成酶（GS）进行了评估。术后2天，视神经挤压伤处的GS活性与未手术对照组织相当，但术后7天和12天增加了30%。相比之下，术后7天和12天，创伤外周神经的GS活性显著低于未手术对照。给予有丝分裂抑制剂（阿糖胞苷，AraC）可防止术后7天时视神经以及术后7天和12天时外周神经中GS活性因创伤而发生显著改变。结果表明，神经纤维损伤后神经胶质/施万细胞GS活性发生显著改变，且给予有丝分裂抑制剂可延迟/预防这些改变。
