Mills Stephen L, Xia Xiao-Bo, Hoshi Hideo, Firth Sally I, Rice Margaret E, Frishman Laura J, Marshak David W
Department of Ophthalmology and Visual Science, University of Texas at Houston-Health Science Center, Houston, Texas 77030, USA.
Vis Neurosci. 2007 Jul-Aug;24(4):593-608. doi: 10.1017/S0952523807070575. Epub 2007 Aug 22.
Many retinal ganglion cells are coupled via gap junctions with neighboring amacrine cells and ganglion cells. We investigated the extent and dynamics of coupling in one such network, the OFF alpha ganglion cell of rabbit retina and its associated amacrine cells. We also observed the relative spread of Neurobiotin injected into a ganglion cell in the presence of modulators of gap junctional permeability. We found that gap junctions between amacrine cells were closed via stimulation of a D(1) dopamine receptor, while the gap junctions between ganglion cells were closed via stimulation of a D(2) dopamine receptor. The pairs of hemichannels making up the heterologous gap junctions between the ganglion and amacrine cells were modulated independently, so that elevations of cAMP in the ganglion cell open the ganglion cell hemichannels, while elevations of cAMP in the amacrine cell close its hemichannels. We also measured endogenous dopamine release from an eyecup preparation and found a basal release from the dark-adapted retina of approximately 2 pmol/min during the day. Maximal stimulation with light increased the rate of dopamine release from rabbit retina by 66%. The results suggest that coupling between members of the OFF alpha ganglion cell/amacrine cell network is differentially modulated with changing levels of dopamine.
许多视网膜神经节细胞通过间隙连接与相邻的无长突细胞和神经节细胞相连。我们研究了这样一个网络中耦合的程度和动态,即兔视网膜的 OFF α 神经节细胞及其相关的无长突细胞。我们还观察了在间隙连接通透性调节剂存在的情况下,注入神经节细胞的神经生物素的相对扩散情况。我们发现,无长突细胞之间的间隙连接通过 D(1) 多巴胺受体的刺激而关闭,而神经节细胞之间的间隙连接通过 D(2) 多巴胺受体的刺激而关闭。构成神经节细胞和无长突细胞之间异源间隙连接的半通道对被独立调节,因此神经节细胞中 cAMP 的升高会打开神经节细胞半通道,而无长突细胞中 cAMP 的升高会关闭其半通道。我们还测量了眼杯制剂中内源性多巴胺的释放,发现白天暗适应视网膜的基础释放量约为 2 pmol/分钟。光的最大刺激使兔视网膜多巴胺释放速率增加了 66%。结果表明,OFF α 神经节细胞/无长突细胞网络成员之间的耦合随着多巴胺水平的变化而受到不同的调节。