It is the underlying assumption of linearity in many feedforward models, then, that leads to the conclusion that inhibition is required to explain cross-orientation buy Ibrutinib suppression. Contrast saturation and response rectification, however, are highly nonlinear. For the test + mask stimulus, the responses of the LGN cells that see no contrast modulation necessarily still

fall to zero. But the responses of those LGN cells that see twice the contrast modulation (e.g., Figure 2H, red neuron) do not double. Their response to the test stimulus itself was already near saturation, so doubling the stimulus contrast increases the cell’s responses only slightly. As a result, the sum of the LGN responses—and therefore the input to the simple cell—falls in the presence of the mask (compare Figures 2I and 2J). Introducing realistic contrast saturation and rectification to an otherwise linear feedforward model results in cross-orientation suppression that is almost identical to that observed in real simple cells. In the model, the depolarization in a simple cell was taken to be proportional to the summed responses of eight LGN cells whose receptive fields were aligned in space. Response saturation and rectification were inserted by drawing the LGN responses from

a database of the recorded responses of cat LGN cells (Priebe and Ferster, 2006). Cross-orientation suppression in the model matched closely the suppression observed in the Vm responses of V1 simple cells: 9% for the high-contrast test gratings and 52% for low-contrast test gratings (Priebe and Ferster,

2006). CDK inhibitor drugs To calculate the corresponding cross-orientation suppression in the spike responses of the model cell, the depolarization CYTH4 evoked by each stimulus was raised to the third power, to simulate the expansive nonlinearity of threshold as smoothed by trial-to-trial variability. The resulting cross-orientation suppression of the model’s spiking responses (29% and 89% for high- and low-contrast test stimuli) is consequently larger than what is predicted for Vm and is comparable to what has been observed experimentally. While nonlinearities in relay cell responses account for the mask-induced reduction in the modulation component of simple cell Vm, these nonlinearities also predict a rise in the mean LGN input to V1 neurons, which is not observed experimentally. This discrepancy might arise in part from synaptic depression at the thalamocortical synapse (Carandini et al., 2002 and Freeman et al., 2002) and because many simple cells receive less than half of their excitatory input from the LGN (Chung and Ferster, 1998 and Ferster et al., 1996). In addition, some of the predictions of this model appear at odds with the interactions between low-contrast test + mask, for which relay cell contrast saturation should have little effect but nonetheless have been reported to interact in cortical complex cells (Busse et al.