Cortical activity changes dramatically upon changes in behavioral state, such as between sleep versus wake (McGinley et al 2015). Though the mechanisms enabling these distinct modes of cortical operation remain largely unknown, inhibitory neurons (INs) have been suggested repeatedly as a regulator of behavioral-state dependent neocortical activity (Batista-Brito et al 2018, Cardin et al 2019, Bugeon et al 2021). Here we investigate how a unique subpopulation of long-range INs impact cortical states. These cells are defined by the co-expression of somatostatin (SST) and neuronal nitric oxide synthase (nNOS), namely SST/nNOS cells. Although they constitute a very small minority of neocortical INs, SST/nNOS cells are evolutionarily old and conserved from reptiles to humans. Further, they have unique morphology for neocortical INs, with long-range projections that span millimeters and cross cortical areas (Tomioka et al 2005).Their remarkably distinctive features and deep evolutionary conservation suggest that SST/nNOS cells play an important role in neocortical function. Until recently, the genetic targeting of SST/nNOS cells has been difficult. We have used intersectional genetic tools to manipulate neocortical SST/nNOS cells in mice to interrogate their in vivo functional roles. Using 2-photon calcium imaging with high precision state monitoring, we find that SST/nNOS cells are specifically active during low-arousal states characterized by low movement and synchronized local field potentials. Using optogenetic manipulation of SST/nNOS cells in combination with in vivo extracellular recordings we show that the activity of SST/nNOS cells is sufficient to induce a synchronized network state, with both increases in low-frequency LFP power and increases in spiking entrainment to these low-frequencies. These observations are specific to SST/nNOS cells as optogenetic activation of SST+/nNOS- cells leads to reduced neocortical network synchrony.