Genetic elimination of rod/cone coupling reveals the contribution of the secondary rod pathway to the retinal output.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 35363529.
- Also identified by DOI 10.1126/sciadv.abm4491 and PMC identifier 10938630.
- Licence recorded as CC BY-NC.
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Abstract
In the retina, signals originating from rod and cone photoreceptors can reach retinal ganglion cells (RGCs)-the output neurons-through different pathways. However, little is known about the exact sensitivities and operating ranges of these pathways. Previously, we created rod- or cone-specific <i>Cx36</i> knockout (KO) mouse lines. Both lines are deficient in rod/cone electrical coupling and therefore provide a way to selectively remove the secondary rod pathway. We measured the threshold of the primary rod pathway in RGCs of wild-type mice. Under pharmacological blockade of the primary rod pathway, the threshold was elevated. This secondary component was removed in the <i>Cx36</i> KOs to unmask the threshold of the third rod pathway, still below cone threshold. In turn, the cone threshold was estimated by several independent methods. Our work defines the functionality of the secondary rod pathway and describes an additive contribution of the different pathways to the retinal output.