Marcus R C, Wang L C, Mason C A
Department of Pathology, Center for Neurobiology and Behavior, College of Physicians and Surgeons, Columbia University, New York 10032, USA.
Development. 1996 Mar;122(3):859-68. doi: 10.1242/dev.122.3.859.
The visual pathway in albino animals is abnormal in that there is a smaller number of ipsilaterally projecting retinal ganglion cells. There are two possible sites of gene action that could result in such a defect. The first site is the retina where the amount of pigmentation in the retinal pigment epithelium is correlated with the degree of ipsilateral innervation (La Vail et al. (1978) J. Comp. Neurol. 182, 399-422). The second site is the optic chiasm, the site of retinal axon divergence. We investigated these two possibilities through a combination of in vivo and in vitro techniques. Our results demonstrate that the growth patterns of retinal axons and the cellular composition of the optic chiasm in albino mice are similar to those of normally pigmented mice, consistent with the albino mutation exerting its effects in the retina, and not on the cells from the chiasmatic midline. We directly tested whether the albino mutation affects the chiasm by studying 'chimeric' cultures of retinal explants and chiasm cells isolated from pigmented and albino mice. Crossed and uncrossed axons from pigmented or albino retinal explants display the same amount of differential growth when grown on either pigmented or albino chiasm cells, demonstrating that the albino mutation does not disrupt the signals for retinal axon divergence associated with the albino optic chiasm. Furthermore, in vitro, a greater proportion of albino retinal ganglion cells from ventrotemporal retina, origin of uncrossed axons, behave like crossed cells, suggesting that the albino mutation acts by respecifying the numbers of retinal ganglion cells that cross the chiasmatic midline.
白化动物的视觉通路是异常的，因为同侧投射的视网膜神经节细胞数量较少。有两个可能的基因作用位点会导致这种缺陷。第一个位点是视网膜，其中视网膜色素上皮中的色素沉着量与同侧神经支配程度相关（La Vail等人，（1978年）《比较神经学杂志》182卷，399 - 422页）。第二个位点是视交叉，即视网膜轴突发散的部位。我们通过体内和体外技术相结合的方式研究了这两种可能性。我们的结果表明，白化小鼠视网膜轴突的生长模式和视交叉的细胞组成与正常色素沉着小鼠相似，这与白化突变在视网膜中发挥作用，而不是对视交叉中线的细胞发挥作用一致。我们通过研究从有色和白化小鼠分离的视网膜外植体和视交叉细胞的“嵌合”培养物，直接测试了白化突变是否影响视交叉。当在有色或白化视交叉细胞上生长时，来自有色或白化视网膜外植体的交叉和未交叉轴突显示出相同程度的差异生长，这表明白化突变不会破坏与白化视交叉相关的视网膜轴突发散信号。此外，在体外，来自颞下视网膜（未交叉轴突的起源）的白化视网膜神经节细胞中，有更大比例的细胞表现得像交叉细胞，这表明白化突变通过重新指定穿过视交叉中线的视网膜神经节细胞数量来发挥作用。
