Williams M A, Piñon L G, Linden R, Pinto L H
Department of Biological Sciences, Purdue University, West Lafayette, IN 47907.
Exp Brain Res. 1990;82(2):393-400. doi: 10.1007/BF00231258.
The time of maximal occurrence of pyknotic nuclei in the retinal ganglion cell layer of postnatal pearl mutant mice is earlier than that in normal mice (Linden and Pinto 1985). Both ganglion and displaced amacrine cells and glia populate the ganglion cell layer. Thus, in order to show that ganglion cells themselves are affected, we counted the numbers of surviving axons in the optic nerve of postnatal day (PND) 0, 4, 12 and adult mice. On PND 0, pearl mutant mice had 139,000 +/- 2800 (SEM) optic axons, about 8% more than wild-type mice (128,000 +/- 1,700; p = 0.031) but on PND 4, pearl mutants had 24% fewer axons than wild-type mice (96,000 +/- 3700 and 119,000 +/- 4600, respectively; p = 0.008). Thus, pearl mutants lose nearly five times as many retinal ganglion cells as wild-type mice in the interval from PND 0 to 4. The number of axons present in adult mice was nearly equal (56,700 +/- 3200 for wild-type and 52,500 +/- 2700 for pearl mutants p = 0.37). We searched for evidence for changes in the schedule of cell death among other neurons of the retina by counting the number of pyknotic nuclei in the various retinal layers. On PND 4, pearl mutant mice had more pyknotic nuclei in the neuroblastic layer than wild-type mice (5000 +/- 400 and 3900 +/- 300, respectively; p less than 0.05). The time-course of the appearance of pyknotic nuclei in the outer nuclear layer differed for the two genotypes (ANOVA, F = 12.5, p less than 0.001). The most striking difference was a greater number of pyknotic nuclei on PND 20 for the pearl mutants (1300) than for wild-type (480; p = 0.002). However, the total number of photoreceptors in adults did not differ between the two genotypes (3.6 x 10(6) +/- 2.4 x 10(5) for wild-type and 3.7 x 10(6) +/- 3.3 x 10(5) for pearl; p greater than 0.8). These results, taken together, show that natural cell death occurs at an earlier time for retinal ganglion cells of pearl mutants, but that the total number of retinal neurons surviving to adulthood is not affected appreciably by the mutation.
产后珍珠突变小鼠视网膜神经节细胞层中固缩核出现的高峰期早于正常小鼠（林登和平托，1985年）。神经节细胞层中既有神经节细胞，也有移位无长突细胞和神经胶质细胞。因此，为了表明神经节细胞本身受到影响，我们对出生后第0天、第4天、第12天的小鼠以及成年小鼠视神经中存活轴突的数量进行了计数。在出生后第0天，珍珠突变小鼠有139,000±2800（标准误）条视神经轴突，比野生型小鼠（128,000±1700；p = 0.031）多约8%，但在出生后第4天，珍珠突变小鼠的轴突比野生型小鼠少24%（分别为96,000±3700和119,000±4600；p = 0.008）。因此，在出生后第0天到第4天期间，珍珠突变小鼠视网膜神经节细胞的损失数量几乎是野生型小鼠的五倍。成年小鼠中存在的轴突数量几乎相等（野生型为56,700±3200，珍珠突变型为52,500±2700，p = 0.37）。我们通过计算视网膜各层中固缩核的数量，寻找视网膜其他神经元细胞死亡时间变化的证据。在出生后第4天，珍珠突变小鼠神经母细胞层中的固缩核比野生型小鼠多（分别为5000±400和3900±300；p＜0.05）。两种基因型在外核层中固缩核出现的时间进程不同（方差分析，F = 12.5，p＜0.001）。最显著的差异是，在出生后第20天，珍珠突变小鼠（1300个）的固缩核数量比野生型小鼠（480个）多（p = 0.002）。然而，两种基因型成年小鼠中光感受器的总数没有差异（野生型为3.6×10⁶±2.4×10⁵，珍珠突变型为3.7×10⁶±3.3×10⁵；p＞0.8）。综合这些结果表明，珍珠突变小鼠的视网膜神经节细胞自然细胞死亡发生得更早，但突变对存活至成年的视网膜神经元总数没有明显影响。
