Lund R D, Lund J S
J Comp Neurol. 1976 Sep 15;169(2):133-54. doi: 10.1002/cne.901690202.
The central visual pathways of the rat have been used as a model for investigating the significance of axonal interactions in mammalian neural development. Attention is restricted largely to the aberrant distribution of optic axons to the ipsilateral side of the brain and their distribution in the superior colliculus after early unilateral eye damage. The normal ipsilateral retinotectal pathway in pigmented rats appears as a series of patches located anteriorly and laterally in the stratum opticum, whereas in albino animals it is a small area lying anteromedially. In both, a few axons are often found at the extreme posterior border of the superior colliculus. After unilateral eye enucleation at birth, an aberrant ipsilateral pathway from the remaining eye arises at the optic chiasm. It originates from all parts of the retina and terminates in the ipsilateral superior colliculus in a topographic fashion such that the upper retina projects laterally and the lower retina, medially. The pathway is heaviest anteromedially (from lower temporal retina) and lightest posterolaterally (from upper nasal retina). There is always a heavy projection to the extreme posterior border of the superior colliculus. In only two animals of a large series was direct intertectal sprouting found. After partial retinal lesions, there is again an ipsilateral pathway from the unlesioned eye which fills the projection area of the lesion. As after total enucleation, the pathway arises from most of the ipsilateral retina, not just that region homotypic to the lesion site, being heaviest from the lower temporal and lightest (or deficient) from the upper retina. There is suggestion of ordering of the projection into the deafferented region in that the ipsilateral degeneration after lesions in the intact eye is compact but does not fill the gap in the crossed projection completely. There is also indication that some intact parts of the retina lesioned at birth may also project in an inappropriate retinotopic fashion to the deafferented region. The corticotectal pathway shows a normal map. Study of the ipsilateral retinotectal pathway indicates that the axons terminating at the extreme posterior border of the superior colliculus arise from the lower temporal retina. The results are interpreted as indicating that the aberrant uncrossed pathways after complete or local retinal lesions, compare very closely in most features. Both distribute to the deafferented area of the superior colliculus -- in one, this is the whole surface, while in the other it is a small area. The fact that in the latter case axons are ending in quite inappropriate parts of the tectal map, may be explained more simply in terms of interactions between adjacent axons in the optic pathway rather than by an hypothesis involving a change in the cell labels across the tectal map.
大鼠的中枢视觉通路已被用作研究轴突相互作用在哺乳动物神经发育中的意义的模型。研究主要集中在早期单侧眼损伤后，视神经轴突向脑同侧的异常分布及其在上丘中的分布。在有色大鼠中，正常的同侧视网膜顶盖通路表现为位于视层前部和外侧的一系列斑块，而在白化动物中，它是位于前内侧的一个小区域。在这两种动物中，通常在上丘的最后缘发现一些轴突。出生时单侧眼球摘除后，来自另一只眼的异常同侧通路在视交叉处形成。它起源于视网膜的各个部位，并以拓扑方式终止于同侧上丘，使得上部视网膜向外侧投射，下部视网膜向内侧投射。该通路在前内侧（来自颞下视网膜）最重，在后外侧（来自鼻上视网膜）最轻。总是有大量投射至上丘的最后缘。在一大组动物中，仅在两只动物中发现了顶盖间的直接发芽。部分视网膜损伤后，未受损眼同样会形成一条同侧通路，填充损伤的投射区域。与完全摘除眼球后一样，该通路起源于同侧大部分视网膜，而不仅仅是与损伤部位同型的区域，从颞下最重，从上部视网膜最轻（或缺乏）。有迹象表明投射到去传入区域存在一定顺序，即完整眼损伤后的同侧变性紧密，但并未完全填充交叉投射中的间隙。也有迹象表明，出生时受损的视网膜的一些完整部分也可能以不适当的视网膜拓扑方式投射到去传入区域。皮质顶盖通路显示出正常的图谱。对同侧视网膜顶盖通路的研究表明在上丘最后缘终止的轴突起源于颞下视网膜。结果被解释为表明完全或局部视网膜损伤后的异常未交叉通路在大多数特征上非常相似。两者都分布到上丘的去传入区域——一种情况是整个表面，而另一种情况是一个小区域。在后一种情况下，轴突终止于顶盖图谱中相当不合适的部位，这一事实可以更简单地用视通路中相邻轴突之间的相互作用来解释，而不是用涉及顶盖图谱中细胞标记变化的假设来解释。
