Early experience plays a key role in the development of the central nervous system as the brain has to adapt continuously to environmental changes that threaten its harmonious development. This adaptation phenomenon is called brain plasticity and refers to the lifelong changes in the structure of the brain that accompany experience (experience-dependent plasticity). Brain plasticity implies that the brain is pliable and can be remolded in response to challenges that interfere with its normal development such as sensory deprivation, brain injury, or abnormal development. Indeed, several regimens of visual deprivation such as dark rearing, enucleation, or eye-lid suturing lead to alterations of the visual system. Conversely, environmental enrichment also produces regional changes in brain anatomy such as increased dendritic space for synapses, increased cortical thickness, and elevated gene expression. Sensory deprivation at birth or perinatally has dramatic effects on the organization of the brain circuitry, leading to a takeover of the deprived cortex by other sensory modalities. This phenomenon is known as cross-modal plasticity and is mediated by the development of new inter-modal connections or by strengthening or unmasking of already existing connections. Cross-modal plasticity has been demonstrated following visual and auditory deprivation since birth. In both cases, the deprived cortex becomes activated by one or more of the remaining senses, touch, audition, and olfact

e visual experience can reshape V1 circuits and thereby enables to improve visual acuity and contrast sensitivity to compensate for the loss of whisker-dependent somatosensation, which in normal rodents provides essential information about their direct environment. 6. Conclusions and Outlook Here, we briefly reviewed the findings of the literature on the cross-modal interplay of primary sensory cortices and on the effects of short-term sensory deprivation on the spared sensory cortical regions. Collectively, the described results suggest that the absence of both audition and somatosensation induces a compensatory improvement of vision. Since primary sensory cortices relay the sensory information to higher-order cortical areas, it would be interesting to investigate how cross-modal modulations as described here are transferred from primary to higher-level cortices and which effects they provoke here. Generally, the fact that the functional cross-modal interplay is present between different sensory cortices across many species raises the question of its relevance for humans or animals. Since it has been suggested that corticocortical connections mediate cross-modal effects [ 1 , 7 – 9 ], further studies are needed to examine how silencing these connections, for example, via optogenetic inactivation, affects multimodal processing at higher-order cortices and, more importantly, sensory-guided behavior in experimental animals. The results of such experiments might reveal new insights into the general relevance of cross-modal integration for sensation and perception. In general, investigations on cross-modal compensatory changes of a spared sensory cortex are rare, and most studies were performed in very young experimental animals. There are first hints that many fundamental mechanisms like LTP, homeostatic plasticity, and synaptic scaling are involved in mediating cross-modal enhancement of the spared senses after deprivation of another sense [ 50 , 59 , 66 , 92 ]. Howev