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金鱼视网膜神经节细胞再生过程中的蛋白质合成与轴突运输因预处理损伤而加速。

Protein synthesis and axonal transport in goldfish retinal ganglion cells during regeneration accelerated by a conditioning lesion.

作者信息

McQuarrie I G, Grafstein B

出版信息

Brain Res. 1982 Nov 11;251(1):25-37. doi: 10.1016/0006-8993(82)91270-7.

DOI:10.1016/0006-8993(82)91270-7
PMID:6184129
Abstract

Axonal outgrowth in goldfish retinal ganglion cells following a testing lesion of the optic axons is accelerated by a prior conditioning lesion. Changes in protein synthesis and axonal transport were examined during the accelerated regeneration. The conditioning lesion was an optic tract cut made 2 weeks prior to the testing lesion, which consisted of a tract cut at the chiasma, so that nerves subjected to either a conditioning lesion ('conditioned nerves') or a sham operation ('sham-conditioned nerves') could be examined in the same animal. In the retinal ganglion cells of conditioned nerves, the incorporation of [3H]proline into protein began to increase between 1 and 8 days after the testing lesion. The amount of fast-transported labeled protein was elevated to about 8 X normal by 1 day after the testing lesion but had decreased to about 3-5X normal at 8 and 22 days. The 8 and 22 day values were not significantly different from those in sham-conditioned nerves or nerves that had received a testing lesion alone. For slow protein transport, the instantaneous amount transported was 15-16 X normal in the conditioned nerves at 1 and 8 days after the testing lesion, and the velocity of slow transport, which was already elevated above normal by 1 day after the testing lesion, was elevated still further by 8 days--to a value in excess of 1.5 mm/day (compared to 0.2-0.4 mm/day in normal animals). We believe that the enhanced outgrowth resulting from the conditioning lesion is due to a transient increase in the amount of fast transport (possibly responsible for a decreased delay in the initiation of sprouting), and a sustained increase in the amount and velocity of slow transport (which may account for an increased rate of elongation).

摘要

金鱼视网膜神经节细胞在视神经轴突进行测试性损伤后,轴突生长会因先前的预处理性损伤而加速。在加速再生过程中,对蛋白质合成和轴突运输的变化进行了检测。预处理性损伤是在测试性损伤前2周进行的视束切断,该切断在视交叉处进行,这样在同一只动物中就可以检查接受预处理性损伤的神经(“预处理神经”)或假手术的神经(“假预处理神经”)。在预处理神经的视网膜神经节细胞中,[3H]脯氨酸掺入蛋白质的过程在测试性损伤后1至8天开始增加。快速运输的标记蛋白质的量在测试性损伤后1天升高到约为正常的8倍,但在8天和22天时降至约为正常的3 - 5倍。8天和22天的值与假预处理神经或仅接受测试性损伤的神经的值没有显著差异。对于慢速蛋白质运输,在测试性损伤后1天和8天,预处理神经中瞬时运输量为正常的15 - 16倍,慢速运输速度在测试性损伤后1天就已高于正常水平,到8天时进一步升高——超过1.5毫米/天(正常动物为0.2 - 0.4毫米/天)。我们认为,预处理性损伤导致的轴突生长增强是由于快速运输量的短暂增加(可能导致发芽起始延迟减少),以及慢速运输量和速度的持续增加(这可能解释了伸长率的增加)。

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