Oxytocin mediates early experience–dependent cross-modal plasticity in the sensory cortices

This study shows that early neonatal sensory deprivation of one modality can impact cortical plasticity of other sensory cortices because of the reduction in dendritic release of oxytocin from paraventricular hypothalamic neurons. The study also shows that exogenous oxytocin can attenuate the effects of neonatal sensory deprivation on cortical plasticity, thus mimicking the beneficial effects of enriched sensory exposure. Sensory experience is critical to development and plasticity of neural circuits. Here we report a new form of plasticity in neonatal mice, where early sensory experience cross-modally regulates development of all sensory cortices via oxytocin signaling. Unimodal sensory deprivation from birth through whisker deprivation or dark rearing reduced excitatory synaptic transmission in the correspondent sensory cortex and cross-modally in other sensory cortices. Sensory experience regulated synthesis and secretion of the neuropeptide oxytocin as well as its level in the cortex. 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 new function for oxytocin in promoting cross-modal, experience-dependent cortical development. This link between sensory experience and oxytocin is particularly relevant to autism, where hypersensitivity or hyposensitivity to sensory inputs is prevalent and oxytocin is a hotly debated potential therapy.