The importance of electrical synapses for brain function has recently come into the limelight. Synaptic contacts of this type are formed between interneurons in several brain regions, prompting the suggestion that electrical coupling is a fundamental feature of local inhibitory circuits. But long before electrical synapses gained this notoriety, their existence in the retina had already captured the attention of many neuroscientists. Electrical synapses are formed between rod amacrine cells (the main output of rod bipolar cells) and cone bipolar cells of the ON pathway. Information from the rod pathway is fed to the cone pathway, partly through this electrical connection. But what is the precise role of electrical synapses in the early stages of visual processing? A recent study by Güldenagel et al. constitutes an important first step to answering this question.

Gap junctions, cellular specializations that bridge the cytoplasm of adjacent cells, are the main structural element of electrical synapses. Gap junctions are formed by a family of proteins called connexins. Only a few connexin types are expressed in the nervous system; in the retina, connexin36 (Cx36) is present in rod amacrine cells, where it forms gap junctions with a different connexin expressed by cone bipolar cells. Güldenagel et al. generated mice lacking Cx36, and explored the effect of this mutation on retinal structure and function. They found that the absence of Cx36 was not accompanied by anatomical abnormalities; all layers of the retina and its central projection seemed normal. In contrast, electroretinographic recordings showed that the so-called 'b-wave', which is related to depolarization of ON-type bipolar cells, was reduced in the mutant mice. Similarly, the latency of light-evoked field potentials recorded in the optic tectum was longer in mutant than in wild-type animals.

So gap junctions are important during early visual processing, as the absence of Cx36 impairs light perception. However, some loose ends must still be tied up. For example, the reduction of the b-wave was observed even if the rod pathway was saturated by light. Under these conditions, ON-type cone bipolar cells are solely driven by cones, and the influence of the rod amacrine cells should be irrelevant in both wild-type and mutant mice. Why, then, is the b-wave smaller under light saturation? A more detailed cellular analysis should give us the answer.