Deprivation of one sensory modality is known to diminish cortical responses in the corresponding sensory cortex as well as alter neuronal responses in unrelated sensory cortices. Yet little is known about what drives this cross-modal plasticity. On page 391, Zheng and colleagues explore the effects of early unimodal sensory deprivation in multiple sensory cortical regions in mice and report that oxytocin, a neuropeptide important for lactation, parturition, social and emotional behaviors, is critical for cross-modal cortical plasticity.
Zheng and colleagues subjected mice to sensory deprivation starting from birth by either removing their whiskers or raising them in the dark. Each type of deprivation decreased spontaneous excitatory synaptic transmission and sensory stimulation-evoked responses in both primary somatosensory (S1) and primary visual (V1) cortex but not in higher order cortical regions such as the prefrontal cortex. This was accompanied by a decrease in oxytocin levels in the sensory cortex affected by the sensory deprivation. Whisker removal or dark rearing also reduced oxytocin production and expression in the hypothalamus. Oxytocin injection into S1 not only increased excitatory synaptic transmission in both S1 and V1 but also reversed the cross-modal effects of sensory deprivation in these areas. To complement their findings from sensory deprivation, Zheng et al. then reared mice in a sensory-enriched environment. This manipulation led to increased oxytocin production in the hypothalamus, higher levels of oxytocin expression in S1 and V1, and enhanced neuronal responses in these cortical areas. Sensory enrichment also rescued the effects of sensory deprivation, similar to the treatment with exogenous oxytocin.
These findings reveal a critical function for oxytocin in activity-dependent cortical development and cortical plasticity.
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Zarate, J. Oxytocin for all senses. Nat Neurosci 17, 340 (2014). https://doi.org/10.1038/nn0314-340