Jansen H G, Sanyal S
Department of Anatomy, Faculty of Medicine, Erasmus University, Rotterdam, The Netherlands.
J Comp Neurol. 1992 Feb 1;316(1):117-25. doi: 10.1002/cne.903160110.
In the retina of mice heterozygous for the retinal degeneration slow gene (rds/+) the photoreceptor cells, both rods and cones, develop abnormal outer segments but establish normal synaptic contacts. The other retinal layers also show normal structural organization. Starting from the age of 2 months, a very slow loss of photoreceptor cells progresses throughout life. As a result, the photoreceptor cell population in the retina of the affected mice is reduced to less than half at the age of 9-18 months. In some of the surviving rod terminals during this period, an increase in the number of synaptic ribbons is recorded. At the same time, the profiles of processes originating from the second order neurons and participating in these synapses are also increased in number so that the multiple ribbons appear as centres of multiple synaptic sites. Morphometric measurements of the perimeter of the synaptic profiles in rod terminals show a significant increase in the rds/+ retina over that of the control retina. Observations based on serial electron microscopy indicate that multiple synaptic sites are developed while the number of the second order neuronal processes, entering the terminals, remains unchanged. The frequency of terminals with multiple synapses in the rds/+ retina increases with progressive photoreceptor cell loss. Similar changes do not occur in the terminals of the cones. It is postulated that loss of some rod photoreceptor cells within a group that is presynaptic to common bipolars or horizontal cells results in partial deafferentation which in turn stimulates the growth of the remaining synaptic elements. The possible compensatory effect and functional significance of such synaptic growth are discussed.
在视网膜变性慢基因（rds/+）杂合的小鼠视网膜中，视杆细胞和视锥细胞这两种光感受器细胞都会发育出异常的外段，但能建立正常的突触联系。视网膜的其他层也显示出正常的结构组织。从2个月大开始，光感受器细胞会非常缓慢地持续丧失，直至终生。结果，在9至18个月大时，受影响小鼠视网膜中的光感受器细胞数量减少到不到一半。在此期间，在一些存活的视杆终末中，记录到突触带数量增加。同时，源自二级神经元并参与这些突触的突起轮廓数量也增加，使得多个突触带呈现为多个突触位点的中心。对视杆终末中突触轮廓周长的形态测量显示，rds/+视网膜中的周长比对照视网膜有显著增加。基于连续电子显微镜的观察表明，在进入终末的二级神经元突起数量保持不变的情况下，多个突触位点得以发育。rds/+视网膜中具有多个突触的终末频率随着光感受器细胞的逐渐丧失而增加。视锥终末中不会出现类似变化。据推测，在与共同双极细胞或水平细胞形成突触前的一组视杆光感受器细胞中，一些细胞的丧失导致部分传入神经阻滞，进而刺激其余突触元件的生长。本文讨论了这种突触生长可能的补偿作用和功能意义。
