Visual transmission deficits in mice with targeted disruption of the gap junction gene connexin36

In the mammalian retina, rods feed into the cone pathway through electroton ic coupling, and recent histological data suggest the involvement of connex in36 (Cx36) in this pathway. We therefore generated Cx36 null mice and moni tored the functional consequences of this deficiency on early visual transm ission. The homozygous mutant mice had a normally developed retina and show ed no changes in the cellular organization of the rod pathway. In contrast, the functional coupling between AII amacrine cells and bipolar cells was i mpaired. Recordings of electroretinograms revealed a significant decrease o f the scotopic b-wave in mutant animals and an increased cone threshold tha t is compatible with a distorted, gap junctional transmission between AII a macrine cells and cone bipolar cells. Recordings of visual evoked potential s showed extended latency in mutant mice but unaffected ON and OFF componen ts. Our results demonstrate that Cx36-containing gap junctions are essentia l for normal synaptic transmission within the rod pathway.