We have shown that mutations in the voltage-gated K+ channel subunit Kv8.2 disrupt photoreceptor adaptation, the fundamental physiological process by which photoreceptor sensitivity is modulated. However, the precise mechanism has yet to be defined. Kv8.2 is the first and, as yet, only voltage-gated K+ channel protein where disease-causing mutations affecting vision have been identified. Our studies are focused on the retinal biology behind Kv8.2 deficiency with the goal to expand our understanding of retinal physiology and disease.
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