Increased slow transport in axons of regenerating newt limbs after a nerve conditioning lesion.
Increased slow transport in axons of regenerating newt limbs after a nerve conditioning lesion.
复制标题
神经调节损伤后再生蝾螈四肢轴突的缓慢运输增加。
DOI：
10.1016/0012-1606(90)90064-p
复制
发表时间：
1990
影响因子：
2.7
通讯作者：
McQuarrie,IG
中科院分区：
文献类型：
--
作者：
Maier,CE;McQuarrie,IG
我们之前已经证明，截肢前两周进行的神经调节损伤（CL）会导致蝾螈的肢体再生更早开始。对鱼类和哺乳动物的研究表明，当 CL 在神经测试病变之前发生时，与未接受 CL 的轴突相比，轴突运输的慢速成分 b (SCb) 会增加。我们想知道 CL 后较早开始的肢体再生是否与 SCb 转运的增加有关。 [35S]蛋氨酸标记的SCb蛋白的转运通过使用SDS-PAGE、荧光照相法和闪烁计数来测量。将[35S]蛋氨酸注射到正常人的运动柱后7、14、21和28天测定SCb蛋白的转运速率和数量；单一病变（即轴索横切术、轴索截肢术或假 CL 后截肢）；和双损伤肢体轴突（即神经横断 CL，两周后进行截肢轴突切除术）。未截肢蝾螈四肢轴突中 SCb 的转运率为 0.19 毫米/天。由于单个损伤，再生轴突中运输的标记 SCb 蛋白数量有所增加，但 SCb 运输速率没有加速，在接受假 CL 和肢体截肢的轴突中，SCb 运输速率为 0.21 毫米/天。当截肢之前进行 CL 时，SCb 转运速率加倍（0.40 毫米/天），并且转运的标记 SCb 蛋白量增加。这项研究表明，CL 后截肢时出现的肢体再生较早与 SCb 蛋白转运增加有关。这表明肢体再生部分受到轴突再生的调节。我们认为，在进入肢体再生的下一阶段之前，芽基需要最少量的神经支配，而 SCb 蛋白的运输决定了何时可以获得该数量。
We have previously shown that a nerve conditioning lesion (CL) made 2 weeks prior to amputation results in an earlier onset of limb regeneration in newts. Studies in fish and mammals demonstrate that when a CL precedes a nerve testing lesion, slow component b (SCb) of axonal transport is increased compared to axons that had not received a CL. We wanted to know whether the earlier initiation of limb regeneration after a CL was associated with an increase in SCb transport. The transport of [35S]methionine labeled SCb proteins was measured by using SDS-PAGE, fluorography, and scintillation counting. The rate of transport and quantity of SCb proteins was determined at 7, 14, 21, and 28 days after injection of [35S]methionine into the motor columns of normal; single lesioned (i.e., transection axotomy, amputation axotomy, or sham CL followed by amputation); and double-lesioned limb axons (i.e., nerve transection CL followed 2 weeks later by amputation axotomy). The rate of SCb transport in axons of unamputated newt limbs was 0.19 mm/day. There was an increase in the amount of labeled SCb proteins transported in axons regenerating as the result of a single lesion but no acceleration in the rate of SCb transport, which was 0.21 mm/day in axons that received a sham CL followed by limb amputation. The rate of SCb transport doubled (0.40 mm/day) and the amount of labeled SCb proteins being transported was increased when amputation was preceded by a CL. This study demonstrates that the earlier onset of limb regrowth, seen when amputation follows a CL, is associated with an increased transport of SCb proteins. This suggests that limb regeneration is, in part, regulated by axonal regrowth. We propose that the blastema requires a minimum quantity of innervation before progressing to the next stage of limb regeneration, and that the transport of SCb proteins determines when that quantity will be available.