Politis M J, Pellegrino R G, Ritchie J M
Brain Res. 1985 Dec 16;359(1-2):187-93. doi: 10.1016/0006-8993(85)91428-3.
Glial and Schwann cells undergo marked biochemical and morphological alterations following axonal injury. In the present experiments, the extent of enzyme activity associated with anaerobic (LDH, lactic dehydrogenase) vs aerobic (SDH, succinic dehydrogenase) respiration was assessed distal to the site of nerve fiber injury. Studies were performed in rat central (optic) and peripheral (sciatic) nerves at 2, 7 and 14 days postoperatively (d.p.o.). In sciatic nerves, LDH activity rose 3-fold in traumatized (vs unoperated control) nerve tissue between 2 and 7 d.p.o. and remained elevated at 14 d.p.o. SDH activity in traumatized nerve was equal to that in unoperated nerve at 7 d.p.o., but decreased at 14 d.p.o. LDH activity in optic nerve at 2 d.p.o. was equivalent to that in control nerve, but rose approximately two-fold by 7 d.p.o. However, unlike peripheral nerve, activity in traumatized optic nerve decreased to control levels at 14 d.p.o. SDH activity in traumatized optic nerve remained unchanged at any timepoint examined. Taken in concert, these data are consistent with the hypothesis that there is an overall shift in CNS glial and Schwann cell metabolism from aerobic to anaerobic respiration following nerve injury. Additional studies were performed to determine if this shift requires prior Schwann or glial cell mitosis. Administration of mitotic inhibitor (AraC, cytosine arabinofuranoside) inhibited post-traumatic elevations in LDH activity in optic, but not peripheral nerve. No significant effect of the drug on axonal degeneration (as assessed by saxitoxin binding) was observed.
轴突损伤后，神经胶质细胞和施万细胞会发生显著的生化和形态学改变。在本实验中，评估了神经纤维损伤部位远端与无氧呼吸（乳酸脱氢酶，LDH）和有氧呼吸（琥珀酸脱氢酶，SDH）相关的酶活性程度。实验在大鼠中枢神经（视神经）和外周神经（坐骨神经）上于术后2天、7天和14天进行。在坐骨神经中，受伤（与未手术对照相比）神经组织中的LDH活性在术后2天至7天之间上升了3倍，并在术后14天仍保持升高。受伤神经中的SDH活性在术后7天时与未手术神经中的相等，但在术后14天时下降。视神经中LDH活性在术后2天时与对照神经中的相当，但到术后7天时上升了约两倍。然而，与外周神经不同的是，受伤视神经中的活性在术后14天时降至对照水平。在任何检测的时间点，受伤视神经中的SDH活性均保持不变。综合来看，这些数据与以下假设一致：神经损伤后，中枢神经系统神经胶质细胞和施万细胞的代谢总体上从有氧呼吸转变为无氧呼吸。还进行了额外的研究以确定这种转变是否需要施万细胞或神经胶质细胞先进行有丝分裂。给予有丝分裂抑制剂（阿糖胞苷，AraC）可抑制视神经而非外周神经创伤后LDH活性的升高。未观察到该药物对轴突变性（通过石房蛤毒素结合评估）有显著影响。
