Furthermore, contrast adaptation enhances information transmission at low contrast (Gaudry and Reinagel, 2007a). In the retina, a major goal is to understand how contrast adaptation arises in the circuitry at the level of synapses and intrinsic membrane properties. Contrast adaptation has been studied in several cell types of salamander retina, including cone photoreceptors and two of their postsynaptic targets: horizontal and bipolar cells. Neither cones nor horizontal www.selleckchem.com/products/Dasatinib.html cells adapt to contrast, and thus contrast adaptation

first appears beyond the point of cone glutamate release (Baccus and Meister, 2002 and Rieke, 2001). Bipolar cells, the excitatory interneurons that transmit cone signals to ganglion cells, do adapt to contrast (Baccus and Meister, 2002 and Rieke, 2001). The bipolar cell’s contrast adaptation is reflected in the excitatory membrane currents and membrane potential (Vm) of ganglion cells (salamander: Baccus and Meister, 2002 and Kim

and Rieke, 2001 and mammal: Beaudoin et al., 2007, Beaudoin et al., 2008, Manookin and Demb, 2006 and Zaghloul et al., 2005). However, this presynaptic mechanism for contrast adaptation explains only a portion of the adaptation in the ganglion cell’s firing rate (Kim and Rieke, Z-VAD-FMK 2001, Zaghloul et al., 2005, Manookin and Demb, 2006 and Beaudoin et al., 2007; 2008). Thus, the presynaptic mechanism combines with intrinsic mechanisms within the ganglion cell to reduce sensitivity during periods of high contrast. In dim light, where signaling depends on rods and rod bipolar cells, contrast adaptation depends predominantly Fossariinae on the ganglion cell’s intrinsic mechanism (Beaudoin et al., 2008). In theory, an intrinsic mechanism for contrast adaptation should sense changes in Vm during high-contrast exposure. During high contrast, a ganglion cell’s Vm spans a wide range and includes periods of both hyperpolarization (up to ∼10 mV) and depolarization (up to ∼20 mV) from

the resting potential (Vrest); the depolarizations are accompanied by increased firing. The durations of hyperpolarizations and depolarizations are determineds by the temporal filtering of retinal circuitry, which under light-adapted conditions shows band-pass tuning with peak sensitivity near ∼8 Hz; this tuning results in brief periods of depolarization and firing (∼50–100 msec) that are themselves separated by ∼100–200 msec (Berry et al., 1997, Zaghloul et al., 2005 and Beaudoin et al., 2007). Therefore, an intrinsic mechanism that suppresses firing at high contrast should recover with a time course longer than the interval between periods of firing; in this way, firing in one period could activate a suppressive mechanism that would affect the subsequent period.