Myall O T, Allen S L, McLean W G
Department of Pharmacology and Therapeutics, University of Liverpool, U.K.
Brain Res. 1990 Jul 23;523(2):295-7. doi: 10.1016/0006-8993(90)91500-g.
Injury of the rat sciatic nerve is accompanied by an increased activity of the enzyme ornithine decarboxylase (ODC) in dorsal root ganglia. This increase is impaired in streptozotocin-induced diabetes, in which retrograde axonal transport of proteins is reduced. In order to confirm the relationship between altered axonal transport and ODC induction we treated rats with acrylamide i.p. to cumulative doses of 150 and 350 mg/kg. One sciatic nerve was crushed under anaesthesia and 24 h later dorsal root ganglia were removed and assayed for ODC activity by a dual-label radioenzymatic method. The ratio of activity of 2.41 +/- 0.57 (crushed side over control side) was reduced to 1.66 +/- 0.9 and 1.7 +/- 0.65 after acrylamide treatment at 150 and 350 mg/kg, respectively. The results are consistent with the postulated role of retrograde axonal transport in the cell body responses to nerve injury and may explain the effect of acrylamide on nerve regeneration.
大鼠坐骨神经损伤时,背根神经节中鸟氨酸脱羧酶(ODC)的活性会增加。在链脲佐菌素诱导的糖尿病中,这种增加受到损害,在该糖尿病模型中蛋白质的逆行轴突运输减少。为了证实轴突运输改变与ODC诱导之间的关系,我们给大鼠腹腔注射丙烯酰胺,累积剂量分别为150和350mg/kg。在麻醉状态下挤压一侧坐骨神经,24小时后取出背根神经节,采用双标记放射酶法检测ODC活性。在150mg/kg和350mg/kg丙烯酰胺处理后,活性比值(损伤侧与对照侧相比)从2.41±0.57分别降至1.66±0.9和1.7±0.65。这些结果与逆行轴突运输在细胞体对神经损伤反应中的假定作用一致,并且可能解释了丙烯酰胺对神经再生的影响。