Jansen H G, Hawkins R K, Sanyal S
Department of Anatomy, Faculty of Medicine, Erasmus University, Rotterdam, the Netherlands.
Microsc Res Tech. 1997 Jan 15;36(2):96-105. doi: 10.1002/(SICI)1097-0029(19970115)36:2<96::AID-JEMT3>3.0.CO;2-T.
Following partial loss of photoreceptor cells in the retina of mice afflicted by mutant genes, damaging light exposure, or old age, some of the remaining rod cells exhibited a process of growth in their synapses with the second order retinal neurons. This growth was recognized by the presence of multiple synaptic sites in some of the rod terminals in the outer plexiform layer. In this study, a comparative analysis of the microanatomical changes in the synaptic structures of the rod terminals in the retina of normal, rds homozygous and heterozygous mutant and light exposed albino mice was undertaken by using a computer-aided three-dimensional reconstruction. A rod terminal normally showed the presence of 1 synaptic complex consisting of a single synaptic ribbon located between 2 processes of horizontal cells and 2 bipolar cell dendrites. In a rod terminal showing an enlarged synaptic complex, 2 or 3 separate synaptic ribbons formed the centres of separate synaptic sites; each of the sites was characterized by the presence of 2 laterally placed horizontal cell processes and 2 bipolar cell dendrites. However, these processes from the multiple synaptic sites were observed to arise from the 2 horizontal and the 2 bipolar cell elements that were normally present in the rod terminal. Thus proliferation of synaptic sites in the rod terminals occurred through growth and sprouting from the processes of the second order neuronal components present within the terminals. The altered synaptic complexes in the variously affected groups were structurally comparable and appeared to have resulted from similar microanatomical changes. The increase in the frequency of rod terminals with multiple synaptic sites occurred as a sequel to increasing photoreceptor cell loss that was recorded at different age points in the different experimental groups. It is concluded that rod synapses in the adult mammalian retina possess structural plasticity that permits compensatory growth.
在因突变基因、光照损伤或衰老而患病的小鼠视网膜中，部分光感受器细胞丧失后，一些剩余的视杆细胞在与二级视网膜神经元的突触处呈现出生长过程。这种生长通过外网状层中一些视杆终末存在多个突触位点得以识别。在本研究中，通过计算机辅助三维重建，对正常、rds纯合和杂合突变以及光照白化小鼠视网膜中视杆终末突触结构的微观解剖学变化进行了比较分析。正常情况下，一个视杆终末有一个突触复合体，由位于两个水平细胞突起和两个双极细胞树突之间的单个突触带组成。在一个显示突触复合体增大的视杆终末中，2个或3个独立的突触带形成了独立突触位点的中心；每个位点的特征是有2个横向排列的水平细胞突起和2个双极细胞树突。然而，观察到来自多个突触位点的这些突起源自视杆终末中通常存在的2个水平细胞和2个双极细胞成分。因此，视杆终末中突触位点的增殖是通过终末内二级神经元成分的突起生长和出芽而发生的。不同受影响组中改变的突触复合体在结构上具有可比性，似乎是由相似的微观解剖学变化导致的。视杆终末具有多个突触位点的频率增加是不同实验组在不同年龄点记录到的光感受器细胞损失增加的结果。得出的结论是，成年哺乳动物视网膜中的视杆突触具有允许代偿性生长的结构可塑性。
