In spite of the fact that our data was taken from brain slices, where many connections have been sectioned, we detect many instances where the connectivity is so dense that it approaches sampling every potential presynaptic input (Figure 8F). Since we randomly chose PCs Docetaxel concentration and also found this dense innervation in pairs or triplets of simultaneously recorded PCs, we interpret our results as indicating that, in principle, every interneuron might be connected to each local. It is unclear

at this point if these results apply only to this population of interneurons in the frontal cortex or whether this very dense connectivity only exists for inhibitory interneurons or is a general feature of cortical connectivity. In any case, future studies need to be performed with other neuronal cell types to address whether our findings are generally applicable. By densely innervating all local PCs, the subpopulation of interneurons that we have studied would affect their function in a global, nonselective manner. This occurs at all developmental stages tested. Although there have been several hypotheses that

have suggested that inhibitory interneurons are involved in crafting specific responses in PCs, such as the generation of specific receptive fields (Runyan et al., 2010), our results are more in line of the idea that inhibition this website serves instead to locally control PCs, perhaps helping stabilize the transfer function of the

circuit, but without a computational function “per se.” This would imply that they themselves are not involved in the generation of specific receptive until field properties (Kerlin et al., 2010). Indeed, the different developmental origin of interneurons, late invaders of cortical territories (Xu et al., 2004) resonates well with an unspecific role, whereby they could arrive late and extend a “blanket of inhibition” throughout the circuit. In finishing, one could reconsider the definition of cortical modules. While there is ample evidence for repetitive features in cortical design at the macroscopic level (“macrocolumns”; Grinvald et al., 1988 and Hubel and Wiesel, 1977), the physical existence of cortical “minicolumns” (Mountcastle, 1982) has been doubted due to the lack of strong anatomical evidence (Crick and Asanuma, 1986). Our results provide a different viewpoint from which to consider cortical modularity. If this type of dense, unspecific connectivity pattern applies to other populations of cortical neurons, neighboring neurons would have overlapping but not identical connectivity patterns. In this scenario, there would be no modules in the cortical microcircuit, but instead each individual neuron defines its own circuit, based on its own distinct input and output innervation.