Oka N, Brimijoin S
Department of Pharmacology, Mayo Clinic, Rochester, MN 55905.
Brain Res. 1990 Feb 12;509(1):107-10. doi: 10.1016/0006-8993(90)90315-3.
To test whether abnormal processing of proteins for fast axonal transport is involved in the neuropathy induced by BPAU (p-bromophenylacetylurea) we examined transport onset. [35S]Methionine was injected into the lumbar ventral horn of rats 2 weeks after BPAU, 400 mg/kg (i.p.) or vehicle. At intervals of 30-90 min consecutive 3-mm segments of the L4 and L5 ventral roots were digested for polyacrylamide gel electrophoresis and fluorography. Fast transported proteins were identified by comparison with samples from mid-thigh sciatic nerve ligated for 16 h after radiolabeling. A prominent 26 kDa band represented the earliest exported protein. It was usually absent at 30 min, but it entered the roots by 45 min. This band was consistently displaced further in BPAU nerve (n = 11) than in controls (n = 11). The mean difference was 5 +/- 0.6 mm (P less than 0.001). However, there was no difference in the apparent velocity of transport. These results imply premature onset of transport in BPAU neuropathy.
为了检测快速轴突运输的蛋白质异常加工是否参与了由BPAU（对溴苯乙酰脲）诱发的神经病变，我们检测了运输起始情况。在给予大鼠腹腔注射400mg/kg BPAU或赋形剂2周后，向大鼠腰髓腹角注射[35S]甲硫氨酸。每隔30 - 90分钟，将L4和L5腹根连续3毫米的节段进行消化，用于聚丙烯酰胺凝胶电泳和荧光显影。通过与放射性标记后结扎16小时的大腿中部坐骨神经样本进行比较，来鉴定快速运输的蛋白质。一条显著的26kDa条带代表最早输出的蛋白质。它通常在30分钟时不存在，但在45分钟时进入神经根。在BPAU处理的神经（n = 11）中，这条带始终比对照组（n = 11）更向近端移位。平均差异为5±0.6毫米（P < 0.001）。然而，运输的表观速度没有差异。这些结果表明在BPAU神经病变中运输起始过早。
