Indeed,

a second possibility is that layer 5 excitatory cells could activate layer 2/3 neurogliaform inhibitory neurons (Xu and Callaway, 2009). Interestingly, a single spike of a neurogliaform cell can elicit long lasting IPSPs mediated by GABAA and GABAB receptors on neighboring cortical pyramids (Tamás et al., 2003), causing diffuse network silencing (Oláh et al., 2009). Finally, layer 5 contains PF-01367338 datasheet also low-threshold spiking interneurons, which send vertically projecting axons to supragranular layers (Xiang et al., 1998). Cell-type-specific inactivation experiments will be required in the near future to dissect among these possibilities. Based on the observed laminar pattern, sound-driven responses PERK inhibitor in V1 could be generated by horizontal cortico-cortical fibers, nonspecific, associative thalamic systems, or ascending neuromodulatory systems that can activate cortical interneurons (e.g., reviewed in Bacci et al., 2005). Nonspecific thalamic systems receive inputs from layer 5 (Jones, 2001 and Theyel

et al., 2010), contain multisensory neurons (Avanzini et al., 1980) and send diffuse axonal projections to supragranular layers, irrespective of cortical boundaries (Jones, 2001). Our transection experiments suggest that sound-driven inhibition is relayed to V1 via cortico-cortical connections between auditory and visual cortices, whose existence has been proven in rodents (Campi et al., 2010 and Laramée et al., 2011). This finding is in agreement with previous reports indicating that widespread interareal influences, as assessed by multisite FP recordings, rely on cortico-cortical connectivity (Amzica and Steriade, 1995 and Frostig et al., 2008). However, we cannot exclude that transections selectively severed thalamo-cortical fibers from higher-order thalamic nuclei, although this seems unlikely. Also, our transection experiments do not

allow to distinguish whether the signal is relayed by direct horizontal connections between A1 and V1 or through an intervening cortical area such as V2, which receives auditory inputs (Laramée et al., 2011). However, the estimated brief latency of about 6 ms elapsing between the activation of A1 and the sound-driven activation of L5Ps in V1 is more compatible with a Histone demethylase role of direct cortico-cortical connections between A1 and V1. Indeed, a 6 ms latency would be consistent with the propagation speed of sensory evoked cortical activity (0.2–0.5 m/s; Benucci et al., 2007), given the distance between A1 and V1 in mice. Our results indicate that sound-driven IPSPs reduce sub- and suprathreshold responsiveness of visual cortical neurons, resulting in a degradation of visually driven, behavioral responses. Cross-modal, GABAergic inhibition has been described so far in the cat ectosylvian cortex (Dehner et al., 2004).