The function of the cerebral cortex relies on the cellular balance between excitatory (pyramidal cells) and inhibitory neurons (interneurons), which is disrupted in disorders such as autism or schizophrenia. The emergence of cortical function during postnatal development relies on spontaneous synchronous activity among large groups of pyramidal cells and interneurons, which later desynchronise for efficient information processing. Before this network activity shift, interneuron numbers are adjusted through activity-dependent programmed cell death mechanisms. However, the extent to which the adjustment in interneuron numbers is required for this change in network dynamics and the identity of specific cell types participating in these events remains to be determined. Here, we address these questions using in vivo functional imaging of the postnatal somatosensory cortex and cell type identification via spatial transcriptomics, in mouse models with impaired developmental cell death of cortical interneurons - thereby assessing the importance of neuronal numbers for the development of cortical function. Using spatial transcriptomics, we first identified the main subtypes of interneurons undergoing developmental cell death in the somatosensory cortex. We further show that sculpting the numbers of these interneuron subtypes through cell death is instrumental in developing neocortical networks: increased interneuron numbers maintain cortical networks at a higher synchronous state across time than controls, leading to a delay in circuit maturation. Our project sheds light on how neuronal diversity and numbers contribute to the emergence of functional circuits, a crucial step for our understanding of physiological and pathological brain wiring.