We mapped receptive fields in the horizontal dimension by presenting sequences of vertical bars (∼10° wide) having random position (six to nine positions, spanning 56°–77° in azimuth)

and polarity (black or white; Figure 1B). A fraction of the bars (usually 8%) were set to zero contrast to obtain blanks (Figure 1A). Each sequence lasted 20 s, and each bar was flashed for 166 or 200 ms. We generated six such sequences and repeated each five times. We used two types of random sequences: balanced and biased. In balanced sequences, the bars were equally likely to appear at any position (Figures 1A and 1B). In biased sequences, the bars were two to three times more likely to appear at a given position selleck chemical than at any of the other positions (Figures 1C and 1D). The number of blanks was kept the same. We fit each cell with a Linear-Nonlinear-Poisson model (LNP model) that maximized the likelihood of the observed spike trains (Paninski, 2004, Pillow, 2007 and Simoncelli et al., 2004). The nonlinearity was imposed to be the same in the balanced and the biased conditions. In this way, differences in tuning and responsiveness between the balanced and biased conditions are entirely captured by the linear filters. We included a constant offset term so that we could allow for changes in mean activity between the two conditions

(Figures 1E and 1H). We fitted two versions of the LNP model for each cell: one in which the linear filter was convolved with a signed version of the stimulus (as appropriate for linear cells), and one RG7204 clinical trial in which it was convolved with an unsigned version of the Thalidomide stimulus (as appropriate for nonlinear cells). For each cell, we chose the version of the model that gave the highest likelihood of the data. We selected the time slice at which the linear filters were maximal to obtain the spatial tuning curve of each neuron (Figure S1). We fitted these responses with Gaussian functions (Figures 1F, 1G, 1I, and 1J) and used the appropriate parameters to quantify response gain, preferred position, and tuning width

for each neuron. We describe the tuning curve of an LGN neuron as: equation(Equation 1) RLGN(φ,θLGN)=f(φ−θLGN)where φφ is the stimulus position and f()f() is the receptive field profile of an LGN neuron with preferred position θLGNθLGN. We can then construct the response of a V1 neuron with preferred position θV1θV1 to the same stimulus as: equation(Equation 2) RV1(φ,θV1)=(∑θLGNRLGN(φ,θLGN)g(θLGN−θV1))αwhere g()g() is the summation profile of the V1 neuron over LGN. This quantity is integrated over all LGN neurons and passed through a static nonlinearity (αα). Effectively, the V1 neuron weights the population response of LGN by its summation profile. To account for our data, it was sufficient to use simple Gaussian functions to describe both f()f() and g()g().