A mean-field model of neural networks with PV and SOM interneurons reveals connectivity-based mechanisms of gamma oscillations.

Classic theoretical models of cortical oscillations are based on the interactions between two populations of excitatory and inhibitory neurons. Nevertheless, experimental studies and network simulations suggest that interneuron subclasses such as parvalbumin (PV) and somatostatin (SOM) exert distinct control over oscillatory dynamics. Yet, we lack a theoretical understanding of the mechanisms underlying oscillations in E-PV-SOM circuits and of the differences with respect to the classical mechanisms for oscillations in simpler E-I networks. Here, we derive a biologically realistic mean-field model of a canonical three-population E-PV-SOM circuit. This model robustly generates oscillations whose features are consistent with experimental observations, including the relative timing of PV and SOM activity and the effects of optogenetic perturbations. By reducing the model to a linear analytical form, we demonstrate that gamma oscillations emerge directly from the cell-specific connectivity of the three-population circuit. This connectivity motif alone accounts for experimentally observed phase relationships, with PV activity consistently leading that of SOM neurons. Together, this mean field model identifies a distinct structural mechanism giving rise to oscillations in canonical E-PV-SOM circuits and provides theoretical primitives for constructing large-scale, cell-type-specific models of cortical dynamics.