Information transfer in mammalian cerebral cortex is dependent on GABAergic interneuron circuits that are widely assumed to be uniform across the neocortex. Here, we demonstrate that this does not hold true during postnatal life prior to the onset of active sensory exploration in mice. During this time, somatostatin interneurons differentially contribute to sensory-evoked activity in primary somatosensory (S1BF) and visual (V1) cortices. In S1BF, somatostatin interneurons provide a mechanism for feedforward control of sensory responses as opposed to the feedback role observed in V1. This functional divergence is explained by differences in both somatostatin subtype and the transient circuits formed by these cells. We propose that the somatosensory circuit represents an adaptation to control early touch information, a key sense for neonatal mice. Further, the presence of distinct, area-dependent GABAergic circuits suggests divergent genetic/molecular programs across different cortices, adding further complexity to our endeavors to understand the etiology of neurodevelopmental psychiatric disorders.