005) above the steady-state response for 2.8 s after the object stopped moving, 12 times longer than their immediate response to the fast motion, which was 233 ms. When one considers the total magnitude of the peripheral increase in activity from sensitization, as measured by the area under the curve (Figure 7B), this was at least as large as (1.1 times) the central decrease in activity caused by adaptation. These results were consistent with the center-surround organization

of their AFs (Figures 1D and 1E). Therefore, following the motion of a camouflaged object, adapting Off (OMS) cells stored and transmitted a prediction of the location of the boundaries of the object after its motion ceased. Guided by the AF model (Figure 2), we tested whether inhibitory neurotransmission was necessary for sensitization. We measured the responses

of sensitizing cells to a uniform-field BIBW2992 datasheet stimulus that changed in contrast during the application of 100 μM picrotoxin, which blocks ionotropic GABAergic receptors. Picrotoxin abolished the ability of these cells to respond during Learly ( Figure 8A) and turned the sensitizing response into an adapting response ( Figure 8B). The change of plasticity was specific to picrotoxin because sensitization persisted in the presence of strychnine, a glycinergic antagonist, and APB, which blocks the On pathway ( Figures S4A and S4B). Thus, GABAergic transmission underlies sensitization, enabling sensitizing ganglion cells to respond quickly MG132 after a contrast decrement. In the AF model, inhibition combines with the excitatory pathway prior to its threshold (Figure 2B). This is necessitated because inhibition delivered after the threshold would produce a vertical shift during sensitization instead of a horizontal shift (Kastner and Baccus, 2011). Such connectivity is most consistent with amacrine cells inhibiting bipolar cell terminals. Salamander bipolar cell

terminals express GABAC receptors that can be blocked by Picrotoxin, but not by Bicuculline, which blocks GABAA receptors found on amacrine GBA3 and ganglion cells (Lukasiewicz et al., 1994). Therefore, our model predicts that sensitization should persist in the presence of Bicuculline, which was indeed the case (Figures 8A and 8B). Previous studies have shown that intracellular recordings of bipolar cells can reveal effects of inhibition at their synaptic terminals, in particular, those bipolar cells that are likely to convey input to OMS cells (Olveczky et al., 2007). Interpreting the excitatory subunits of the AF model to be bipolar cells, the model predicts that, during Learly, bipolar cell terminals receive less steady inhibition than during Llate. As previously reported ( Baccus and Meister, 2002 and Rieke, 2001), we found that some bipolar cells had a hyperpolarized membrane potential during Learly compared to Llate. However, we also found bipolar cells with a depolarized membrane potential during Learly compared to Llate ( Figures 9A and 9B).