This finding suggests that, besides the phase difference between pyramidal cells and inhibitory interneurons, local groups of neurons (as captured by a MUA recording) are locked to approximately the same phase of the gamma rhythm.

This leaves a cell’s position in the horizontal cortical map or vertical cortical column as the main candidate determinants of its preferred gamma phase. A position in the horizontal cortical map, during visual stimulation, translates to a particular position in the cortical activation map. A given selleck inhibitor stimulus typically generates an ordered spatial pattern of activation in the map, such that a cell’s position in the map translates into a particular activation level. We have shown previously that

the level of V1 activation further translates to the gamma phase (Vinck et al., 2010a). However, this effect accounted INCB024360 mouse for only a relatively small part of the phase variance (see Figure 2 of Vinck et al., 2010a). The activation independent part of the phase variance (that is already visible in that figure and replicated here in Figure 4) likely requires a different explanation. We propose that it is related to the remaining possible source of phase variance, i.e., the position of a neuron in the vertical cortical column. In fact, there is direct evidence in favor of this suggestion: Livingstone (1996) has shown that pairs of gamma-synchronized neurons within the granular and supragranular layers of monkey V1 had the more superficial neuron lagging the deeper neuron by ∼3 ms for a distance of ∼400 μm. The dependence of gamma phase on the vertical position in the cortex might be due to the pattern of synaptic connections within a column and the resulting flow of activation. Gamma

activity is primarily found in supragranular layers (Buffalo et al., 2011), and within those, the gamma phase of firing increases systematically with distance from the input layer 4 (Livingstone 1996). At the same time, a larger distance from layer 4 corresponds to a longer conduction time. Thus, the precise others connectivity of the cortical column might generate the precise temporal sequence of gamma activation. Therefore, we would like to suggest that a cell’s preferred gamma phase is determined by two activation-independent factors (vertical position and cell class) and one activation-dependent factor (cf. gamma phase shifting). The interplay between these contributions to the gamma phase might explain the firing sequences and their stimulus dependence in anesthetized cat primary visual cortex (Havenith et al., 2011). The potential consequences of the different gamma-phase components are intriguing. First, the delay between pyramidal cell and interneuron spiking allows the gamma rhythm and in fact overall activation to be maintained (Börgers and Kopell, 2005).