Cellular & molecular origins of the electro‐oculogram

Abstract

AbstractThe clinical electro‐oculogram has been used to assess retinal pigment epithelium (RPE) function using the changes in the standing potential of the eye in response to light. However, only a part of this mechanism is fully understood. One important clinical finding is that individuals with Best’s macular dystrophy display a reduced light‐rise and therefore a role for bestrophin in the generation of the light‐rise is necessary. It is now evident that bestrophin acts a regulator of intracellular calcium stores interacting with the L‐type‐Ca2+ channel in the basolateral membrane of the RPE to drive the changes in basolateral chloride conductance. This new role helps to explain the cases of Best’s macular dystrophy in which the light‐rise is normal. However, the initiating events surrounding the rise in intracellular calcium are unknown. One possibility is that light itself is able to elevate intracellular Inositol tri‐phosphate that releases calcium from intracellular stores and initiate the light‐rise. The talk will elaborate on the role of bestrophin in the generation of the light‐rise, and examine light and the onset of phagocytosis as possible triggers for the light‐rise.