Brain circuits in mouse pups develop and mature extensively during the first few weeks of life. During early postnatal development, sensory cortices experience patterned spontaneous activity which is known to refine neural connectivity, preparing the animal to engage in sensorimotor tasks immediately upon ear and eye opening (∼P4 and ∼P15, respectively). In primary visual cortex (V1), spontaneous activity originates from two sources, from the retina relayed by thalamus and intrinsically generated in the cortex. Spontaneous events from these two sources have different spatiotemporal properties: the retina-driven L-events with low synchronicity and low cell participation and the intrinsic H-events with high synchronicity and increased cell participation. Perturbation of this activity consequently leads to miswiring of the developing nervous system and likely contributes to neurodevelopmental disorders. Using a spiking network model of excitatory (E) population and two inhibitory populations, i.e. parvalbumin-expressing (PV) and somatostatin-expressing (SST) interneurons, we investigated the effect of modulating inhibition on spontaneous activity dynamics in V1. The model recapitulated experimental findings where SST activation reduces correlation and firing rates of E neurons, while SST inhibition leads to increased cell recruitment to L-events. Furthermore, the model predicted that PV hypoactivation leads to an increased percentage of H-events, consistent with experiments in Fragile X Syndrome (FXS) mice. We also explored co-modulating PV and SST cells simultaneously. We found that SST cells control L-event spatial structure, whereas PV cells significantly influence on the temporal correlation. Altogether, our model provides insight into spontaneous activity dynamics in developing V1 and can apply to other similarly developing sensory cortices.