Baldridge W H, Ball A K, Miller R G
Division of Anatomy and Experimental Morphology, McMaster University, Hamilton, Ontario, Canada.
J Comp Neurol. 1989 Sep 8;287(2):238-46. doi: 10.1002/cne.902870207.
The I1 dopaminergic interplexiform cells of the fish retina are believed to modulate horizontal cell coupling by increasing gap junction resistance. Dopamine also modulates the morphology of horizontal cell gap junctions and mimics the effects of light adaptation. To determine whether the light-dependent changes in gap junction morphology are due to endogenous dopamine release, horizontal cell gap junctions were studied in goldfish retinas lacking dopaminergic neurons. Dopaminergic interplexiform cells were destroyed by intraocular injections of 6-hydroxydopamine in both eyes. After lesioning, fish were treated in one of four ways: (1) light-adapted, (2) dark-adapted (1 hour), (3) light-adapted and given an intraocular injection of dopamine, or (4) dark-adapted (1 hour) and injected with dopamine. The effectiveness of lesioning was evaluated by autoradiographic detection of [3H]-dopamine uptake in the retina of one eye. Retinas in which lesioning of the contralateral eye was deemed effective were processed for freeze-fracture electron microscopy and the particle density of horizontal cell gap junctions determined. Lesioned retinas, whether light- or dark-adapted, had elevated horizontal cell soma gap junction particle densities compared to lesioned retinas treated with dopamine. These results demonstrate that high soma gap junction particle densities can be correlated with the absence of dopamine and low densities associated with the presence of dopamine. The differences in gap junction particle density between lesioned and lesioned + dopamine-treatment were similar to differences between nonlesioned dark-adapted (1 hour) and light-adapted retinas, respectively. Therefore, the particle density of light- and dark-adapted soma gap junctions suggests a greater release of dopamine in light-adapted fish than in 1 hour dark-adapted fish.(ABSTRACT TRUNCATED AT 250 WORDS)
鱼类视网膜中的I1多巴胺能网间细胞被认为可通过增加缝隙连接电阻来调节水平细胞耦合。多巴胺还可调节水平细胞缝隙连接的形态,并模拟光适应的效果。为了确定缝隙连接形态的光依赖性变化是否源于内源性多巴胺释放,研究人员在缺乏多巴胺能神经元的金鱼视网膜中对水平细胞缝隙连接进行了研究。通过向双眼眼内注射6-羟基多巴胺来破坏多巴胺能网间细胞。损伤后,将鱼分为以下四种处理方式之一:(1)光适应,(2)暗适应(1小时),(3)光适应并眼内注射多巴胺,或(4)暗适应(1小时)并注射多巴胺。通过放射自显影检测一只眼睛视网膜中[3H]-多巴胺摄取来评估损伤的有效性。对侧眼损伤被认为有效的视网膜进行冷冻断裂电子显微镜处理,并确定水平细胞缝隙连接的颗粒密度。与用多巴胺处理的损伤视网膜相比,无论是光适应还是暗适应的损伤视网膜,其水平细胞体缝隙连接颗粒密度均升高。这些结果表明,高的体细胞缝隙连接颗粒密度与多巴胺的缺失相关,而低密度与多巴胺的存在相关。损伤视网膜与损伤+多巴胺处理视网膜之间的缝隙连接颗粒密度差异分别类似于未损伤的暗适应(1小时)和光适应视网膜之间的差异。因此,光适应和暗适应体细胞缝隙连接的颗粒密度表明,光适应鱼体内多巴胺的释放量比暗适应1小时的鱼更多。(摘要截短至250字)