PV and SOM cells play distinct causal roles in controlling network oscillations and stability

The causal roles of parvalbumin (PV)- and somatostatin (SOM)-positive interneurons in regulating cortical oscillations and stability remain unclear. We developed a biologically grounded microcircuit model composed of excitatory (E), PV, and SOM neurons that explains key experimental findings, including the precise phase locking of PV cells, delayed firing of SOM cells, and the distinct effects of optogenetic perturbations. By perturbing the spike timing of cells while preserving their firing rates, we show that network oscillations depend on the precise timing of both PV and SOM cells: PV cells regulate oscillation frequency and network stability, while SOM cells control oscillation amplitude. Asymmetric PV-SOM connectivity is essential for generating stochastic gamma oscillations by establishing distinct interneuron timing. Increasing SOM density along the hierarchy predicts decreasing oscillation frequencies and increased seizure susceptibility. Our findings suggest a unified circuit model for oscillations across frequency bands, revealing distinct yet synergistic roles of PV and SOM interneurons.