Early loss of a given sensory input in mammals causes anatomical and functional modifications in the brain via a process called cross-modal plasticity. In the past four decades, several animal models have illuminated our understanding of the biological substrates involved in cross-modal plasticity. Progressively, studies are now starting to emphasise on cell-specific mechanisms that may be responsible for this intermodal sensory plasticity. Inhibitory interneurons expressing γ-aminobutyric acid (GABA) play an important role in maintaining the appropriate dynamic range of cortical excitation, in critical periods of developmental plasticity, in receptive field refinement, and in treatment of sensory information reaching the cerebral cortex. The diverse interneuron population is very sensitive to sensory experience during development. GABAergic neurons are therefore well suited to act as a gate for mediating cross-modal plasticity. This paper attempts to highlight the links between early sensory deprivation, cortical GABAergic interneuron alterations, and cross-modal plasticity, discuss its implications, and further provide insights for future research in the field. 1. Introduction Patterns of activity from the peripheral sensory receptor arrays can dramatically influence the development of connectivity and functional organization of cortical fields in mammals. In some species, evolution in relation to specific environmental cues has nurtured the brain’s blueprint in such a way that a sensory cortex processing specific survival needs has been enlarged over time as compared to other modalities (Figure 1) [1–5]. Similarly, when a sensory function is lost during development, spared senses compensate by taking more cortical space and recruiting the deafferented areas, to maintain homeostasis of sensory function. This reorganization optimizes and secures the individual’s survival and awareness to future environmental changes. For example, the loss of sight at birth or during early life in humans leads to important anatomical and functional reorganization of the visually deprived cortex that will become activated by a wide variety of nonvisual stimuli involving touch, audition, and olfaction [6–11]. Enhanced spatiotemporal functions in the remaining sensory modalities have also been reported [12–16]. It seems therefore that the visual cortex of the blind is not lifeless and is capable of adapting in order to accommodate these nonvisual inputs through cross-modal plasticity. Figure 1: Primary cortical areas in three species of mammals (i.e., Mouse, Ghost Bat and
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