INTRA-CRANICAL TRANSECTION OF THE OPTIC-NERVE IN ADULT MICE - PRELIMINARY-OBSERVATIONS

INTRA-CRANICAL TRANSECTION OF THE OPTIC-NERVE IN ADULT MICE - PRELIMINARY-OBSERVATIONS
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DOI:
10.1016/0014-4886(82)90212-6
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发表时间:
1982-01-01
影响因子:
5.3
通讯作者:
INGOGLIA, NA
INGOGLIA, NA
中科院分区:
医学2区
文献类型:
--
作者:
GRAFSTEIN, B;INGOGLIA, NA

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在小鼠视神经的颅内横切后1-3天之间,视网膜神经节细胞的数量减少约20%,细胞的平均横截面积减少约25%。数量下降持续较慢,2-3个月时降至正常值的50-60%,而平均细胞大小在约30天后开始恢复,到90天时变得接近正常。在视神经的视网膜残端中,银染色切片显示完全轴突变性的核心区域从病变向眼睛延伸约1.5 mm的距离。该核心在病变后1天已经存在,可能是由于病变视网膜侧的神经缺血所致。退化的核心被大约25-40 μ m厚的覆盖层包围,覆盖层含有完整的轴突,推测轴突通过从神经表面扩散而得到营养。外套层约占总神经横截面的30%。从第8天开始,退化的核心获得了一群中等厚度的纤维,这些纤维可能是结缔组织的组成部分,尽管它们不能肯定地与再生轴突区分开来。在损伤后的任何时间都没有轴突再生的可疑证据。视网膜残端中的一些幸存轴突显示出终末球,但这些终末球的发育程度低于颅侧残端中轴突退化前病变的颅侧。轴突运输可能受损,即使在视网膜残端的幸存轴突。这可能是阻止再生的重要因素。
Between 1-3 days after intracranial transection of the mouse optic nerve, the number of retinal ganglion cells decreased by about 20% and the mean cross-sectional area of the cells decreased by about 25%. The decrease in number continued more slowly, to 50-60% of normal by 2-3 mo., whereas the mean cell size began to recover after about 30 days, becoming nearly normal by 90 days. In the retinal stump of the optic nerve, Ag-stained sections showed a core region of complete axonal degeneration extending for a distance of about 1.5 mm from the lesion toward the eye. This core, which was already present 1 day after the lesion, was probably due to ischemia of the nerve on the retinal side of the lesion. The degenerated core was surrounded by a mantle layer, about 25-40 .mu.m in thickness, containing intact axons which were presumably nourished by diffusion from the surface of the nerve. The mantle layer represents about 30% of the total nerve cross section. Beginning at 8 days the degenerated core acquired a population of moderately thick fibers, which were probably constituents of connective tissue, although they could not be distinguished with certainty from regenerating axons. There was no equivocal evidence of axonal regeneration at any time after the lesion. Some of the surviving axons in the retinal stump showed terminal bulbs, but these were less well developed than those seen on the cranial side of the lesion before the axons in the cranial stump degenerated. Axonal transport might be impaired even in the surviving axons in the retinal stump. This may be a significant factor in deterring regeneration.