Retinal light responsiveness measured via electroretinography undergoes developmental modulation, and is thought to be critically regulated by both visual experience and dopamine. The primary goal of this study was to determine whether dopamine D2 receptors regulate the visual experience-dependent functional development of the retina. Accordingly, we recorded electroretinograms from wild-type mice and mice with a genetic deletion of the gene that encodes the D2 receptor raised under normal cyclic light conditions and constant darkness. Our results demonstrate that D2 receptor mutation preferentially increases the amplitude of the inner retinal light responses evoked by high-intensity light measured as oscillatory potentials in adult mice. During postnatal development, all three major components of electroretinograms, i.e. a-waves, b-waves, and oscillatory potentials, increase with age. Comparatively, D2 receptor mutation preferentially reduces the age-dependent increase in b-waves evoked by low-intensity light. Light deprivation from birth reduces b-wave amplitudes and completely abolishes the increased amplitude of oscillatory potentials of D2 receptor mutants. Taken together, these results demonstrate that D2 receptors play an important role in the activity-dependent functional development of the mouse retina.
We investigated whether dopamine D2 receptor regulates the activity-dependent functional development of the retina using ERG recordings. Our results demonstrate that mutation of the dopamine D2 receptors increases the amplitudes of ERG OPs in adults and reduces the developmental increase of ERG b-waves. In addition, light deprivation from birth completely diminishes the increased amplitude of OPs in D2−/− mice, demonstrating that the dopamine D2 receptor plays an important role in the activity-dependent functional development of the mouse retina.