It could be the synaptic mechanism behind the cross-modal suppressive interactions shown with extracellular recordings

in ferrets (Bizley et al., 2007) and macaques (Kayser et al., 2008 and Lakatos et al., 2007). Interestingly, cross-modal deactivations have been described also in human occipital cortex using neuroimaging (Laurienti et al., 2002). Albeit we give evidence that the majority of V1 neurons are inhibited by sound, we also found that this is due to acoustic-driven excitation of few infragranular cells. This observation is consistent with other reports of spiking responses driven by heteromodal stimuli in primary sensory areas ( Bizley et al., 2007, Morrell, 1972 and Wallace et al., 2004). In line with our findings, such responses are mostly restricted to deep cortical laminae in rodents ( Wallace et al., 2004). Protein Tyrosine Kinase inhibitor Long-range recruitment of inhibitory subcircuits could be a way to control the fluctuations of subthreshold neural activity in early sensory cortices (Cardin et al., 2009 and Traub et al., 1996), and therefore their phase of excitability. In fact, cross-modal Obeticholic Acid purchase modulation of responsiveness in early cortices depends on stimulus onset asynchrony,

indicating a time-dependent modulation of cortical excitability induced by heteromodal stimulation (Lakatos et al., 2007). This type of interaction plays a key role in sensory coding, since cross-modal modulation of oscillatory activity in early sensory areas is supposed to add information about external stimuli (Kayser et al., 2010)

by providing a time reference to spikes. SHs resetted the phase of ongoing V1 activity and were often followed by a depolarization of the cell. Interestingly, when visual stimuli were presented during the depolarizing plateau, visual responsiveness increased (G.I. and P.M., unpublished data). The GABAergic silencing of local network activity driven by heteromodal stimuli could be the condition allowing the phase-resetting of ongoing activity observed extracellularly by our and other groups (Lakatos et al., 2007). What is the functional significance of SHs in V1? First, the fact that activation of a primary cortex by a salient stimulus (such as a noise burst in A1) degrades neuronal also processing in neighboring areas is in line with the idea that sensory cortices compete for the activation of higher cortical areas. The steep emergence of SHs with increasing sound intensities suggests that, for interareal inhibition to be effective, a certain threshold of activation of A1 has to be reached, particularly to affect the animal’s behavior. The fact that SHs were evoked robustly for intensity larger than 55–60 dB SPL is in line with the view that an acoustic stimulus has to be salient for this mechanism to be recruited. Second, it is tempting to speculate that heteromodal inhibition could modulate the selectivity of visual cortical neurons for stimulus attributes such as orientation.