Tomey D A, Heckroth J A
Indiana University School of Medicine, Terre Haute Center for Medical Education 47809.
Exp Neurol. 1993 Jul;122(1):165-70. doi: 10.1006/exnr.1993.1117.
Injection of cell suspensions of normal embryonic cerebellar tissue into adult and juvenile lurcher mutant mice results in infiltration of the atrophic host cerebellar cortex by genetically normal Purkinje cells, as has previously been observed in Purkinje cell degeneration (pcd) mutant mice. In lurcher, the grafted Purkinje neurons most frequently occupy the host molecular layer and produce axons which, in some cases, invade the host cerebellar nuclei. The grafted Purkinje neurons fail to adopt their characteristic planar dendritic disposition in lurcher hosts, probably because of the severe depletion of cerebellar granule neurons and parallel fibers in this mutant. Results reported previously in pcd mutants have thus been extended, with some deviations, to a similar but genetically distinct hereditary cerebellar atrophy, providing evidence of the generalized nature of the phenomena involved.
将正常胚胎小脑组织的细胞悬液注射到成年和幼年的蹒跚突变小鼠体内，会导致基因正常的浦肯野细胞浸润萎缩的宿主小脑皮质，这与之前在浦肯野细胞变性（pcd）突变小鼠中观察到的情况相同。在蹒跚突变小鼠中，移植的浦肯野神经元最常占据宿主分子层并产生轴突，在某些情况下，这些轴突会侵入宿主小脑核。移植的浦肯野神经元在蹒跚突变宿主中未能形成其特征性的平面树突排列，这可能是因为该突变体中小脑颗粒神经元和平行纤维严重缺失。因此，之前在pcd突变体中报道的结果已在一定程度上扩展到了一种类似但基因不同的遗传性小脑萎缩，为所涉及现象的普遍性提供了证据。
