GABAergic interneurons shape the way the brain processing information in many ways. Why interneurons present themselves as a veritable zoo of cell types, however, is not resolved. I will present a hypothesis for a functional role for a widespread network motif consisting of parvalbumin- (PV), somatostatin- (SOM) and vasoactive intestinal peptide (VIP)-expressing interneurons. Following the idea that PV and SOM interneurons control the distribution of somatic and dendritic inhibition onto PCs, I will suggest that mutual inhibition between VIP and SOM cells translates weak inputs to VIP interneurons into large changes of somato-dendritic inhibition of PCs. My means of computational modeling, I will show that the neuronal and synaptic properties of the circuit support this hypothesis, and that the SOM-VIP motif allows transient inputs to persistently switch the circuit between two processing modes, in which top-down inputs onto apical dendrites of PCs are either integrated or canceled.