Dopamine regulates the membrane potential and glycine release of AII amacrine cells via D1-like receptor modulation of gap junction coupling.

Dopamine plays a pivotal role in adjusting the flow of information across the retina as luminance changes from night to day. Here we show, under dim photopic conditions, that both dopamine and a D1-like receptor (D1R) agonist hyperpolarized the resting membrane potential (Vm) of AII amacrine cells (AII-ACs). Surprisingly, in the presence of glutamatergic and GABAergic synaptic blockers that isolate glycinergic synapses, D1R agonists are without effect. However, a D1R antagonist depolarized Vm and reduced the input resistance of AII-ACs in wild type mice, but not in Cx36-/- mice. Accordingly, D1R antagonists enhanced tonic glycinergic transmission to type-2 OFF-cone bipolar cells (OFF-CBCs). D1Rs thus adjust the Vm and excitability of AII-ACs and, thereby, the level of glycine release to OFF-CBCs by regulating gap junction coupling with ON cone bipolar cells. Our findings provide insights into how the retina may use dopamine to adapt crossover inhibitory microcircuits during changes in luminance.