Rod Vision Is Controlled by Dopamine-Dependent Sensitization of Rod Bipolar Cells by GABA

SummaryDark and light adaptation of retinal neurons allow our vision to operate over an enormous light intensity range. Here we report a mechanism that controls the light sensitivity and operational range of rod-driven bipolar cells that mediate dim-light vision. Our data indicate that the light responses of these cells are enhanced by sustained chloride currents via GABAC receptor channels. This sensitizing GABAergic input is controlled by dopamine D1 receptors, with horizontal cells serving as a plausible source of GABA release. Our findings expand the role of dopamine in vision from its well-established function of suppressing rod-driven signals in bright light to enhancing the same signals under dim illumination. They further reveal a role for GABA in sensitizing the circuitry for dim-light vision, thereby complementing GABA's traditional role in providing dynamic feedforward and feedback inhibition in the retina.

► The sensitivity of rod-driven vision is regulated by dopamine and GABA
► The effect of dopamine is conveyed via D1 receptors
► Dopamine stimulates sustained GABAergic input onto rod bipolar cells
► GABA sensitizes rod bipolar cells via GABAC receptors