Lu Bin, Coffey Peter, Lund Raymond
Department of Ophthalmology and Visual Science, Moran Eye Center, University of Utah Health Science Center, 75 N. Medical Drive, Salt Lake City, UT 84132, USA.
Brain Res. 2004 Oct 29;1025(1-2):220-5. doi: 10.1016/j.brainres.2004.06.081.
In most subcortical visual centers in normal mice maintained for a period in the dark, very few neurons express fos-like immunoreactivity (FLI), most likely reflecting c-fos expression, but if an animal is exposed to a flashing light, there is transient increase in the number of FLI-expressing cells. In dark-maintained retinal degeneration (rd) mice, with an inherited photoreceptor defect, numbers of FLI-positive cells, identified immunohistochemically, are anomalously elevated in the superior colliculus (SC) and lateral geniculate nucleus (LGN). Eye removal largely prevents the elevated counts. The difference in number of FLI-positive cells in the SC of rd mice and nondystrophic controls is highly significant (p<0.001). Because we have previously found a similar phenomenon in Royal College of Surgeons (RCS) rats, in which photoreceptor loss is caused by a retinal pigment cell defect, it argues for an effect related to photoreceptor loss rather than its cause.
在黑暗环境中饲养一段时间的正常小鼠的大多数皮层下视觉中枢中,很少有神经元表达类Fos免疫反应性(FLI),这很可能反映了c-fos的表达,但如果动物暴露于闪烁光下,表达FLI的细胞数量会短暂增加。在患有遗传性光感受器缺陷的黑暗饲养的视网膜变性(rd)小鼠中,通过免疫组织化学鉴定,上丘(SC)和外侧膝状体核(LGN)中FLI阳性细胞的数量异常增加。摘除眼球在很大程度上可防止细胞数量增加。rd小鼠和非营养不良对照小鼠的SC中FLI阳性细胞数量差异非常显著(p<0.001)。因为我们之前在皇家外科学院(RCS)大鼠中也发现了类似现象,其光感受器丧失是由视网膜色素细胞缺陷引起的,这表明这种效应与光感受器丧失有关,而非其原因。