Burmeister D W, Grafstein B
Brain Res. 1985 Feb 18;327(1-2):45-51. doi: 10.1016/0006-8993(85)91497-0.
Injury to the optic axons of goldfish elicits dramatic changes in the cell bodies of the neurons from which these axons arise, the retinal ganglion cells. The changes include a large increase in cell size and in synthesis and axonal transport of protein. The cells begin to return to normal about 3 weeks after the injury, when the axons invade the contralateral (homotopic) lobe of the optic tectum, and recovery is essentially complete by 8-10 weeks after the lesion. However, if the homotopic lobe of the tectum was removed at the time of nerve crush, we found that the cell body reaction was greatly prolonged. The cells remained enlarged, and [3H]proline incorporation and fast axonal transport of protein remained elevated, until at least 10-12 weeks after nerve crush, although by this time most of the regenerating axons had probably regained their normal length and many had entered the remaining ipsilateral (heterotopic) lobe of the tectum. The cells showed partial recovery by the latest time tested, 26 weeks after nerve crush, when the projections from the two eyes had segregated into separate bands in the heterotopic tectal lobe.
金鱼视神经轴突损伤会引发这些轴突所源自的神经元(即视网膜神经节细胞)胞体的显著变化。这些变化包括细胞大小大幅增加,以及蛋白质合成和轴突运输增加。损伤后约3周,当轴突侵入视顶盖的对侧(同位)叶时,细胞开始恢复正常,损伤后8 - 10周恢复基本完成。然而,如果在神经挤压时切除顶盖的同位叶,我们发现胞体反应会大大延长。细胞仍然肿大,[3H]脯氨酸掺入和蛋白质的快速轴突运输仍然升高,直到神经挤压后至少10 - 12周,尽管此时大多数再生轴突可能已恢复正常长度,许多轴突已进入顶盖剩余的同侧(异位)叶。在神经挤压后最晚测试时间(26周),当来自双眼的投射在异位顶盖叶中分离成单独的条带时,细胞显示出部分恢复。