Abstract：
Gap junctions are channels that allow for direct transmission of electrical signals between cells. However, the ability of one cell to be impacted or controlled by other cells through gap junctions remains unclear. In this study, heterocellular coupling between ON α retinal ganglion cells (α-RGCs) and displaced amacrine cells (ACs) in the mouse retina was used as a model. The impact of the extent of coupling of interconnected ACs on the synchronized firing between coupled ON α-RGC-AC pair was investigated using the dopamine 1 receptor (D1R) antagonist-SCH23390 and agonist-SKF38393. It was observed that the synchronized firing between the ON α-RGC-ACs pairs was increased by the D1R antagonist SCH23390, whereas it was eradicated by the agonist SKF38393. Subsequently, the signaling drive was investigated by infecting coupled ON α-RGC-AC pairs with the channelrhodopsin-2(ChR2) mutation L132C engineered to enhance light sensitivities. The results demonstrated that the spikes of ON α-RGCs (without ChR2) could be triggered by ACs (with ChR2) through the gap junction, and vice versa. Furthermore, it was observed that ON α-RGCs stimulated with 3-10 Hz currents by whole cell patch could elicit synchronous spikes in the coupled ACs, and vice versa. This provided direct evidence that the firing of one cell could be influenced by another cell through gap junctions. However, this phenomenon was not observed between OFF α-RGC pairs. The study implied that the synchronized firing between ON α-RGC-AC pairs could potentially be affected by the coupling of interconnected ACs. Additionally, one cell type could selectively control the firing of another cell type, thereby forcefully transmitting information. The key role of gap junctions in synchronizing firing and driving cells between α-RGCs and coupled ACs in the mouse retina was highlighted.NEW & NOTEWORTHY This study investigates the role of gap junctions in transmitting electrical signals between cells and their potential for cell control. Using ON α retinal ganglion cells (α-RGCs) and amacrine cells (ACs) in the mouse retina, the researchers find that the extent of coupling between ACs affects synchronized firing. Bidirectional signaling occurs between ACs and ON α-RGCs through gap junctions.
摘要：
间隙连接是允许在细胞之间直接传输电信号的通道。然而,一个细胞通过间隙连接受其他细胞影响或控制的能力尚不清楚。在这项研究中,使用小鼠视网膜中ONα视网膜神经节细胞（RGC）和移位的无长突细胞（AC）之间的异源偶联作为模型。研究了互连AC的耦合程度对耦合ONαRGC-AC对之间同步点火的影响。观察到，多巴胺1受体拮抗剂SCH23390增加了ONαRGC-AC对之间的同步放电，而激动剂SKF38393则根除了它。随后，偶联的ONαRGC-AC对感染了通道视紫红质2（ChR2）突变L132C。ONαRGCs(不含ChR2)的尖峰可以由AC(含ChR2)通过间隙连接触发,反之亦然。此外，观察到，全细胞贴片用3-10Hz电流刺激的ONαRGC可以在耦合的AC中引起同步尖峰，反之亦然。研究表明，ONαRGC-AC对之间的同步点火可能会受到互连AC耦合的影响，另一种细胞类型可以选择性地控制一种细胞类型的发射，信息可以被强行传递。强调了间隙连接在同步小鼠视网膜中αRGC和偶联AC之间的放电和驱动细胞中的关键作用。
