Abstract
BackgroundLoss of a sensory function is often followed by the hypersensitivity of other modalities in mammals, which secures them well-awareness to environmental changes. Cellular and molecular mechanisms underlying cross-modal sensory plasticity remain to be documented.Methodology/Principal FindingsMultidisciplinary approaches, such as electrophysiology, behavioral task and immunohistochemistry, were used to examine the involvement of specific types of neurons in cross-modal plasticity. We have established a mouse model that olfactory deficit leads to a whisking upregulation, and studied how GABAergic neurons are involved in this cross-modal plasticity. In the meantime of inducing whisker tactile hypersensitivity, the olfactory injury recruits more GABAergic neurons and their fine processes in the barrel cortex, as well as upregulates their capacity of encoding action potentials. The hyperpolarization driven by inhibitory inputs strengthens the encoding ability of their target cells.Conclusion/SignificanceThe upregulation of GABAergic neurons and the functional enhancement of neuronal networks may play an important role in cross-modal sensory plasticity. This finding provides the clues for developing therapeutic approaches to help sensory recovery and substitution.
Highlights
Human beings with the loss of a sensory function appear hypersensitive to other stimuli, such as blindness individuals demonstrate the enhanced touch and auditory functions for spatial identification, and deaf ones are alert to visual input for their communications [1,2,3,4,5,6]
To detect whisker tactile sensation, we measured the frequency of free-air whisking, which denotes active tactile sensation, and the duration of whiskers’ retraction after puffing air toward them, which stands for tactile sensitivity to stimulations (Fig. 1)
To understand cellular mechanisms underlying this cross-modal plasticity from olfactory deficit to whisker tactile upregulation, we examined changes in the morphology and functions of GABAergic neurons in barrel cortex
Summary
Human beings with the loss of a sensory function appear hypersensitive to other stimuli, such as blindness individuals demonstrate the enhanced touch and auditory functions for spatial identification, and deaf ones are alert to visual input for their communications [1,2,3,4,5,6] In these types of cross-modal sensory plasticity, the hypersensitivity in the remained sensory modalities and subsequent sensory substitution maintain the homeostasis in sensory functions and well-awareness to living environments. Cross-modal sensory plasticity in rodents is accompanied by the enlargement of cortical areas for remained modalities [3,5,7,8], the high expression of certain genes [9,10] and the rewire/ crosswire of neural circuits [7] It is not known about its cellular mechanisms. Cellular and molecular mechanisms underlying cross-modal sensory plasticity remain to be documented
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