靠近核周的树突横断后神经元存活或死亡:与电生理、形态学和超微结构变化的相关性。

J H Lucas, G W Gross, D G Emery, C R Gardner
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引用次数: 83

摘要

我们研究了在核周400微米范围内树突横切损伤后单层培养小鼠脊髓神经元存活的概率。在650个受损神经元的基础上,我们进行了以下观察。首先,神经元存活是病变与核周的距离和病变部位的突起直径的函数。对于平均直径为3微米的病变,50微米、100微米和150微米处的树突横断分别与30%、53%和70%的存活率相关。其次,损伤细胞的命运在损伤后24小时确定,很可能早在2小时就确定了。第三,导致细胞死亡的早期恶化阶段与光镜下的细胞质相亮度有关,与电镜下大量小的、电子发光的空泡和肿胀的线粒体的出现有关。这些垂死细胞的细胞质染成黑色,不含可见的微管或神经丝。第四,在躯体上记录的损伤电位的大小和时间过程是病变距离的函数,并且在横断后30分钟内没有恢复到病变前的水平。损伤后24小时,损伤神经元的平均膜电位比对照神经元低8%。第六,在大约300微米的损伤距离上,损伤电位和细胞死亡的概率都接近于零。我们得出结论,在使用的模型系统中,树突截肢后的神经元存活取决于病变的物理参数,这些参数决定了到达体细胞的损伤电流的大小。如果损伤发生在离细胞体250微米的范围内,则不能保证存活;如果损伤发生在离胞体50微米的范围内,则有可能导致细胞死亡。损伤后24小时低于正常的膜电位表明,恢复中的神经元可能更容易受到继发性损伤。线粒体断裂和微管丢失的特征表明,损伤电流中的钙成分有助于细胞死亡。
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Neuronal survival or death after dendrite transection close to the perikaryon: correlation with electrophysiologic, morphologic, and ultrastructural changes.

We investigated the probability of survival of mouse spinal neurons in monolayer cultures after transection lesions of dendrites made within 400 microns of the perikarya. Based on a total of 650 lesioned neurons, the following observations were made. First, neuronal survival is a function of lesion distance from the perikaryon and of process diameter at the lesion site. For an average lesion diameter of 3 microns, dendrite transections at 50 microns, 100 microns, and 150 microns were associated with survival probabilities of 30%, 53%, and 70%, respectively. Second, the fate of the injured cells was definitely established 24 hours after injury and very likely was determined as early as 2 hours. Third, early stages of deterioration leading to cell death were associated with cytoplasmic phase brightness on light microscopy, correlating with an appearance of numerous, small, electron-lucent vacuoles and swollen mitochondria on electron microscopy. The cytoplasm of these moribund cells stained darkly and contained no visible microtubules or neurofilaments. Fourth, the magnitude and time course of injury potentials recorded at the somata were a function of the lesion distance and did not return to prelesion levels within 30 minutes after transection. Fifth, at 24 hours after injury, the average membrane potential of lesioned neurons was 8% below that of control neurons. Sixth, at a lesion distance of approximately 300 microns both the injury potential and the probability of cell death approach zero. We conclude that, in the model system used, neuronal survival after dendrite amputation depends on physical parameters of the lesion that determine the magnitude of the injury current reaching the soma. Survival is not assured if the injury is inflicted within 250 microns of the cell body, and cell death is likely for lesions within 50 microns of the soma. The below-normal membrane potentials at 24 hours after injury suggest a possible greater vulnerability of recovering neurons to secondary insults. The characteristic mitochondrial disruption and loss of microtubules implies that the calcium component of the injury current contributes to cell death.

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