The effects of adaptation in V1 neurons were manifestly different: receptive field profiles showed a marked repulsion (Figures 2E–2H). This repulsion distorted the relationship between stimulus position and preferred position (Figure 2F). The maximum repulsion occurred for V1 cells with receptive field profiles peaking ∼5° away from the adaptor (Figure 2H). The receptive field profiles of these cells were shifted

by ∼3.5°. Given the typical Enzalutamide ic50 tuning width (full-width at half-height [FWHH]) of 21°, this equates to a shift of ∼17%. These marked shifts in preference were accompanied by small changes in response gain (Figure 2G) and minor changes in tuning width (data not shown). These effects did not seem to depend on cortical layer and appeared to be weaker in some putative inhibitory interneurons, as judged by spike width (Figure S2). How can the same kind of adaptation regime impact two adjacent stages of processing so differently? One possibility is that adaptation changes the way that V1 operates on signals from the LGN. In particular, perhaps it changes the way that V1 neurons summate their LGN inputs, enhancing the contribution of LGN neurons tuned for positions that are distant from the

adaptor. Alternatively, V1 might be unaware of spatial adaptation and inherit it entirely from the changes that adaptation causes in LGN. Indeed, even if the summation rules between LGN and V1 remained fixed, mafosfamide V1 neurons would integrate over different profiles of LGN activity depending on the adaptation Selleck Perifosine condition. If this “cascade hypothesis” could account for the data, it would be preferable for its parsimony. The cascade hypothesis was indeed sufficient to account for the data (Figures 2I–2L). We considered a fixed summation model where V1 neurons obtain their spatial selectivity through a weighted sum of the appropriate LGN inputs, with

weights that are not adaptable. We then applied this model to LGN responses determined from our measurements (Figure 2I). The predicted V1 responses (Figure 2J) closely resembled the measured ones (Figure 2F): they showed a mild reduction in gain at the adaptor position (Figure 2K) and a clear repulsion of the tuning curves away from that position (Figure 2L). Overall, the model accounted for ∼98% of the variance in the V1 responses, and the residuals (data not shown) did not show much structure. The fixed summation model, therefore, provides a good account of the effects of spatial adaptation in V1. To illustrate the workings of the model, consider its predictions for the responses of a V1 neuron to two stimuli (Figure 3). Take first a stimulus that is close to the adaptor, 3° away. This stimulus elicits a profile of LGN activity that is barely affected by adaptation (Figure 3A).