Delayed-Rectifier K Channels Contribute to Contrast Adaptation in Mammalian Retinal Ganglion Cells

SummaryRetinal ganglion cells adapt by reducing their sensitivity during periods of high contrast. Contrast adaptation in the firing response depends on both presynaptic and intrinsic mechanisms. Here, we investigated intrinsic mechanisms for contrast adaptation in OFF Alpha ganglion cells in the in vitro guinea pig retina. Using either visual stimulation or current injection, we show that brief depolarization evoked spiking and suppressed firing during subsequent depolarization. The suppression could be explained by Na channel inactivation, as shown in salamander cells. However, brief hyperpolarization in the physiological range (5–10 mV) also suppressed firing during subsequent depolarization. This suppression was selectively sensitive to blockers of delayed-rectifier K channels (KDR). In somatic membrane patches, we observed tetraethylammonium-sensitive KDR currents that activated near −25 mV. Recovery from inactivation occurred at potentials hyperpolarized to Vrest. Brief periods of hyperpolarization apparently remove KDR inactivation and thereby increase the channel pool available to suppress excitability during subsequent depolarization.

► Brief hyperpolarization of retinal ganglion cells suppresses future excitability
► Hyperpolarization-induced suppression depends on delayed-rectifier K channels
► Delayed-rectifier K channels generate contrast adaptation in ganglion cells
► Sodium channel inactivation generates contrast adaptation in mammalian ganglion cells