The mammalian retina is a specialized neural circuit of the central nervous system that enables vision: it detects light, processes images, and transmits visual information to higher brain centers. Retinal ganglion cells (RGCs) are the output neurons of the retina that form the optic nerve and relay visual information via spike patterns. RGC dysfunction or death leads to irreversible vision loss, highlighting its essential role for vision. Ion channels are key modulators of the electrical properties of RGCs underlying their responses to visual stimuli. Little is known, however, about how voltage-gated potassium (Kv) channels that typically regulate neuronal excitability contribute to RGC function and synaptic connectivity within the mammalian retina. Single-cell RNA sequencing reveal that the murine ON-sustained (ON-sus) “alpha” RGC (αRGC) subtype, which are the primary RGC type encoding for light increments, robustly express Kv1.1 channels. Whether Kv1.1 channels have roles in circuit establishment of the retina or contribute to the passive and/or active membrane properties of αRGCs and synaptic function remains unknown. Using a murine model with constitutive Kv1.1 knockout targeted to αRGCs, electrophysiology, pharmacology, and high-resolution confocal imaging, we demonstrate a novel role for Kv1.1 channels in regulating the spiking pattern of ON-sus αRGCs.
Stevens-Sostre et al. (Sun,) studied this question.