Fig. 7.

Sources of inhibition to rod bipolar cells under dark-adapted conditions and upon D1 receptor activation. A: in dim light, rod bipolar cells receive reciprocal inhibition from A17 amacrine cells (1) and lateral inhibition from wide-field GABAergic amacrine cells (2), as well as narrow-field glycinergic amacrine cells (not shown). When light stimuli of sufficient size are used, the strength of lateral inhibition to rod bipolar cells (2) is diminished by serial inhibition (3). B: when D1 receptors are activated, this circuit is modified at several sites: ON bipolar cell voltage-gated sodium (NaV) channels are inactivated (1), potentially affecting glutamate release onto downstream targets. The strength of serial inhibition is increased (2), either through greater release of GABA by wide-field amacrine cells onto other amacrine cells or the potentiation of GABA_A currents in cells that are targets of serial inhibition. GABA release by amacrine cells that mediate lateral inhibition (3) is decreased independent of serial inhibitory influences, possibly through D1-dependent modulation of NaVs or voltage-gated calcium (CaVs). ONL, outer nuclear layer; OPL, outer plexiform layer; INL, inner nuclear layer; IPL, inner plexiform layer; GCL, ganglion cell layer; R, rod photoreceptor; C, cone photoreceptor; RB, rod bipolar cell; Glu, glutamate; ⌂, D1 receptor.