产前x射线照射后大鼠视觉系统的发育

G. Brückner , V. Mareš , D. Biesold
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引用次数: 3

摘要

孕16或19天的大鼠(孕16或19天)用100r辐照,24小时后或24、180天处死。x射线的主要影响是位于脑室周围区的细胞以及脑实质中一些分化程度较高的细胞的致死性病变。ed16照射后,大脑皮层和上丘(SC)的急性损伤大于外侧膝状核(LGN)。ed19的照射主要损害视觉系统的皮质部分。因此,急性损伤的程度与视觉中枢的组织和细胞分化程度成反比(br ckner等)。1976)。在成年动物急性辐射损伤导致包装密度和神经元总数的缺陷。在ED 16照射的动物显示皮层深层(lvi)的变化比浅层更明显。SC的缺陷较小,LGN的神经细胞堆积密度增加。在ED 19照射的动物中,神经元密度的缺陷主要发生在皮层的较浅层,最大的缺陷发生在第iv层。从急性和最终变化的比较可以得出结论,成神经细胞前细胞群的损伤在胚胎发育后期得到补偿,而在早期成神经细胞阶段引起的损伤是不可逆的,并导致永久性缺陷。神经胶质细胞数量的变化与髓磷脂缺乏区神经元数量的变化类似,而在髓磷脂丰富区,神经胶质细胞的数量似乎取决于传出和传入神经纤维数量的变化。
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Development of rat visual system after prenatal X-irradiation

Rats pregnant for 16 or 19 days (ED 16 or 19) were irradiated with 100 r and killed after 24 hrs or at age 24 or 180 days. The primary influence of X-rays consists in a lethal lesion of cells located in the periventricular zone as well as some of the more differentiated cells in the brain parenchyma. After irradiation on ED 16, the acute damage was greater in the cerebral cortex and the superior colliculus (SC) than in the lateral geniculate nucleus (LGN). Irradiation on ED 19 damaged mainly the cortical part of the visual system. The degree of acute damage is therefore inversely proportional to the degree of histo- and cytodifferentiation of the visual centres (Brückner et ai. 1976).

In adult animals the acute radiation damage results in a deficit in packing density and the total number of neurons. Animals irradiated on ED 16 revealed more pronounced changes in deep layers of the cortex (L VI) than in the superficial layers. The deficit was smaller in the SC, and in the LGN an increase in the packing density of nerve cells was found. In animals irradiated on ED 19, the deficit in neurons density occurred mainly in more superficial layers of the cortex, with a maximum deficit in layer IV.

From comparison of acute and final changes it may be concluded that the damage of preneuroblastic cell populations is compensated during later embryonic development, while the damage induced in populations already at early neuroblast stage is irreversible and leads to a permanent deficit.

Glia cell population is altered in a similar way as the number of neurons in regions poor in myelin, while in regions rich in myelin the number of glia cells seems to depend on changes in the number of efferent and afferent nerve fibres.

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