Sensory experience is critical to development and plasticity of neural circuits. Here, we report a novel form of plasticity in neonatal mice, where early sensory experience crossmodally regulates development of all sensory cortices via oxytocin signaling. Unimodal sensory deprivation from birth through whisker-deprivation or dark-rearing reduced excitatory synaptic transmission both in the correspondent sensory cortex, and crossmodally in other sensory cortices. Sensory expression regulated synthesis and secretion of the neuropeptide oxytocin, as well as its cortical level. Importantly, both in vivo oxytocin injection and increased sensory experience elevated excitatory synaptic transmission in multiple sensory cortices, and significantly rescued the effects of sensory deprivation. Together, these results identify a novel function for oxytocin in promoting crossmodal, experience-dependent cortical development. This link between sensory experience and oxytocin is particularly relevant to autism, where hyper- or hyposensitivity to sensory inputs is prevalent and oxytocin is a hotly debated potential therapy.