This was done by first binning the spikes of all neurons at 100 ms. Binning spikes at 100 ms removes high-frequency oscillations, and thus correlations seen in the plots are low-frequency correlations. This was a similar analysis as was used in Goard & Dan (2009). We then used the MATLAB routine corrcoef to compute the correlation coefficient for a subset of 80 neurons taken from all layers (20 neurons per layer) in RF1 and RF2 across trials in both the control and the stimulated cases. To see how attention, mAChR stimulation and BF stimulation changed correlations between cells, in Figs 8 and 9 we plot the excitatory–excitatory, excitatory–inhibitory and inhibitory–inhibitory correlations for the six

non-control

conditions discussed above (indicated selleck inhibitor by the row name). For each of the nine subplots in Figs 8 and 9, the non-control condition is plotted on the y-axis against the control condition, plotted on the x-axis. Each scatter point corresponds to the correlation value computed under both the non-control (y-axis) and control (x-axis) conditions. Thus, a scatter point above the line y = x indicates an increase in correlation in the non-control condition. A scatter point below the line y = x indicates a decrease in correlation in the non-control condition. Black and blue scatter points are used for RF1 and RF2, respectively. Red and green crosses indicate the center of mass of the scatter points for RF1 and RF2, respectively, and the size of the crosses is 20 times the standard error of the mean (SEM) of the center of mass. We first

analysed the between-cell correlations during BF stimulation. A similar study was find more performed experimentally on rats by Goard & Dan (2009). In their study, the BF was periodically stimulated (similar to Rebamipide ours) while showing the rats a natural movie. They found that during periods of BF stimulation, the neurons in V1 became decorrelated. In addition, they showed that this correlation is mediated by muscarinic receptors. As can be seen in the bottom row of Fig. 8, when we stimulated the BF, excitatory–inhibitory and inhibitory–inhibitory correlations in both RF1 and RF2 decreased, while excitatory–excitatory correlations remained unchanged. Our result suggests that the decorrelation reported by Goard and Dan was primarily mediated by inhibitory neurons. For the mAChR in RF1 case (middle row of Fig. 8), we also see a decrease in between-cell correlations, indicating that the decrease in correlations is further mediated by mAChRs. We also applied top-down attentional signals to our cortical columns and saw how this affected between-cell correlations with and without mAChR and BF stimulation (Fig. 9). Attentional modulation is classically known to increase firing rates in a particular subset of neurons in order to bias these neurons so they win out in competition against other groups (Desimone & Duncan, 1995).