To meet the high energy demands of photoreceptor cells, the outer retina metabolizes glucose through glycolytic and oxidative pathways resulting in large scale production of lactate and CO₂. Mct3, a proton-coupled monocarboxylate transporter is critically positioned to facilitate transport of lactate and H⁺ out of the retina and could therefore play a role in pH and ion homeostasis of the outer retina. Mct3 is preferentially expressed in the basolateral membrane of the retinal pigment epithelium and forms a heteromeric complex with the accessory protein CD147. To examine the physiological role of Mct3 in the retina, we generated mice with a targeted deletion in Mct3 (slc16A8). The overall retinal histology of 4-36 week old Mct3^-/- mice appeared normal. In the absence of MCT3 expression of CD147 was lost from the basolateral, but not apical RPE. The saturated a-wave amplitude (amax) of the scotopic electroretinogram (ERG) was reduced by ~2 fold in Mct3^-/- mice relative to wild type mice. A 4-fold increase in lactate in the retina suggested a decrease in outer-retinal pH. In single-cell recordings from superfused retinal slices saturating amplitudes of single rod photocurrents (J_max) were comparable indicating that Mct3^-/- mouse photoreceptor cells were inherently healthy. Based on these data, we hypothesize that disruption of Mct3 leads to a potentially reversible decrease in subretinal space pH, thereby reducing the magnitude of the light suppressible photoreceptor current.