ACCELERATION OF AXONAL OUTGROWTH IN RAT SCIATIC-NERVE AT ONE WEEK AFTER AXOTOMY

ACCELERATION OF AXONAL OUTGROWTH IN RAT SCIATIC-NERVE AT ONE WEEK AFTER AXOTOMY
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DOI:
10.1002/neu.480240308
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发表时间:
1993-03-01
期刊:
JOURNAL OF NEUROBIOLOGY
影响因子:
--
通讯作者:
MCQUARRIE, IG
MCQUARRIE, IG
中科院分区:
其他
文献类型:
--
作者:
JACOB, JM;MCQUARRIE, IG

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在大鼠坐骨神经运动轴突损伤后,如果有预先的“条件性”轴突切断,轴突生长的速度会更快。生长的加速是由于SCb的加速,SCb是轴突运输的速率[慢(SC)]组分,其携带细胞基质蛋白;这在条件性轴突切断术后7天发生在整个轴突中(Jacob和McQuarrie,1991 a,J.Neurobiol.2004,2005)。22:570-583)。为了进一步表征条件损伤效应(CLE),重要的是要知道(1)最小有效条件间隔(条件损伤和测试损伤之间的时间),(2)是否需要细胞体反应,以及(3)在单次轴突切断后生长是否加速。通过放射性标记所有新合成的神经元蛋白质并检测通过快速轴突运输携带到生长锥的蛋白质来测量向外生长距离。当同时进行调节和测试损伤时(0天调节间隔),没有CLE。在调节间隔3天的情况下,在生长速率没有变化的情况下,初始延迟(在生长开始之前)缩短。与调理间隔7,14和21天,生长率分别增加了8%,22%和11%,分别。为了确定是否轴突切断的细胞体反应是必要的CLE,nonaxotomizing刺激轴突生长(部分去神经支配)被用来代替一个条件性轴突切断。这对14天后进行的测试病变的生长速率没有影响。最后,我们研究了一个单一的病变后生长加速的可能性。轴突切断后6-9天的生长速度比3-6天快(p < 0.001),9-12天进一步加速(p < 0.001)。我们的结论是:(1)最短的有效的调节间隔是3天;(2)细胞体反应是必要的CLE;(3)轴突生长从一个单一的轴突切断加速与细胞体反应的合成代谢相一致。反过来,SCb马达也被这种反应上调。这表明SCb马达响应于作为细胞体反应产物的快速传输信号。
Following injury of sciatic motor axons in the rat, the rate of axonal outgrowth is faster if there has been a prior ''conditioning'' axotomy. The acceleration of outgrowth is due to an acceleration of SCb, the rate [slow (SC)] component of axonal transport that carries cytomatrix proteins; this occurs throughout the axon by 7 days after the conditioning axotomy (Jacob and McQuarrie, 1991a, J. Neurobiol. 22:570-583). To further characterize the conditioning lesion effect (CLE), it is important to know (1) the minimum effective conditioning interval (time between conditioning and testing lesions), (2) whether the cell body reaction is required, and (3) whether outgrowth accelerates after a single axotomy. Outgrowth distances were measured by radiolabeling all newly synthesized neuronal proteins and detecting those carried to growth cones by fast axonal transport. When the conditioning and testing lesions were made simultaneously (0 day conditioning interval), there was no CLE. With a conditioning interval of 3 days, there was a shortening of the initial delay (before the onset of outgrowth) without a change in outgrowth rate. With conditioning intervals of 7, 14, and 21 days, the rates of outgrowth were increased by 8%, 22%, and 11%, respectively. To determine whether the cell body reaction to axotomy is necessary for the CLE, a nonaxotomizing stimulus to axonal growth (partial denervation) was used in place of a conditioning axotomy. This had no effect on the rate of outgrowth from a testing lesion made 14 days later. Finally, we examined the possibility that outgrowth accelerates after a single lesion. Outgrowth was faster at 6-9 days after axotomy than at 3-6 days (p < 0.001), and accelerated further at 9-12 days (p < 0.001). We conclude that (1) the shortest effective conditioning interval is 3 days; (2) the cell body reaction is necessary for the CLE; (3) axonal outgrowth from a single axotomy accelerates in concert with the anabolic phase of the cell body reaction. The SCb motor is, in turn, upregulated by this reaction. This suggests that the SCb motor responds to a fast-transported signal that is a product of the cell body reaction.