Bloomfield S A, Xin D, Osborne T
Department of Ophthalmology, New York University Medical Center, New York 10016, USA.
Vis Neurosci. 1997 May-Jun;14(3):565-76. doi: 10.1017/s0952523800012220.
The rod-driven, AII amacrine cells in the mammalian retina maintain homologous gap junctions with one another as well as heterologous gap junctions with on-cone bipolar cells. We used background illumination to study whether changes in the adaptational state of the retina affected the permeabilities of these two sets of gap junctions. To access changes in permeability, we injected single AII amacrine cells with the biotinylated tracer, Neurobiotin, and measured the extent of tracer coupling to neighboring AII cells and neighboring cone bipolar cells. We also measured the center-receptive field size of AII cells to assess concomitant changes in electrical coupling. Our results indicate that in well dark-adapted retinas, AII cells form relatively small networks averaging 20 amacrine cells and covering about 75 microns. The size of these networks matched closely to the size of AII cell on-center receptive fields. However, over most of their operating range, AII cells formed dramatically larger networks, averaging 326 amacrine cells, which corresponded to an increased receptive-field size. As the retina was light adapted beyond the operating range of the AII cells, they uncoupled to form networks comparable in size to those seem in well dark-adapted retinas. Our results, then, indicate that the adaptational state of the retina has a profound effect on the extent of electrical coupling between AII amacrine cells. Although we observed light-induced changes in the number of tracer-coupled cone bipolar cells, these appeared to be an epiphenomenon of changes in homologous coupling between AII amacrine cells. Therefore, in contrast to the robust changes in AII-AII coupling produced by background illumination, our data provided no evidence of a light-induced modulation of coupling between AII cells and on-cone bipolar cells.
在哺乳动物视网膜中,由视杆驱动的AII无长突细胞彼此之间保持着同源性缝隙连接,同时与视锥双极细胞保持着异源性缝隙连接。我们利用背景光照来研究视网膜适应状态的变化是否会影响这两组缝隙连接的通透性。为了检测通透性的变化,我们向单个AII无长突细胞注射了生物素化示踪剂神经生物素,并测量示踪剂与相邻AII细胞及相邻视锥双极细胞的耦联程度。我们还测量了AII细胞的中心感受野大小,以评估电耦联的相应变化。我们的结果表明,在充分暗适应的视网膜中,AII细胞形成相对较小的网络,平均包含20个无长突细胞,覆盖范围约为75微米。这些网络的大小与AII细胞的中心型感受野大小紧密匹配。然而,在其大部分工作范围内,AII细胞形成的网络显著增大,平均包含326个无长突细胞,这与感受野大小的增加相对应。当视网膜适应光照超过AII细胞的工作范围时,它们会解耦联,形成与充分暗适应视网膜中所见大小相当的网络。因此,我们的结果表明,视网膜的适应状态对AII无长突细胞之间的电耦联程度有深远影响。尽管我们观察到光照引起了示踪剂耦联的视锥双极细胞数量的变化,但这些似乎是AII无长突细胞之间同源耦联变化的附带现象。因此,与背景光照引起的AII - AII耦联的显著变化形成对比的是,我们的数据没有提供光照诱导AII细胞与视锥双极细胞之间耦联调节的证据。