**3.4 Vestibular-somatosensory interactions**

The vestibular cortex differs from other sensory cortices in that vestibular signals are distributed in an extensive network of cortical regions [40–42]. A wholebrain electrophysiological investigation using galvanic vestibular stimulation and fMRI mapping described the cortical projections of vestibular inputs to functionally diverse cortical regions that included S1 [43] (rat). In addition, a more recent investigation revealed that the optogenetic stimulation of the medial vestibular nucleus neurons elicited bilateral fMRI activations in the sensorimotor cortices and their thalamic nuclei [44] (rat). Nevertheless, which region of S1 receives vestibular inputs and how the bimodal interplay occurs has not yet been investigated. In a recent study in rat, we reasoned that the vestibulo-somatosensory convergence in S1 could occur in the cortical zones of the paw representations that would be

congruent with the functional role of these inputs in posturo-locomotor regulation. Accordingly, we evaluated the immediate effects of a complete unilateral vestibular neurectomy on the response properties of S1 neurons in the hindpaw cutaneous representations [45]. We found that the acute deafferentation immediately induces a bilateral expansion of the cutaneous receptive fields that exclusively concerned those located on the plantar skin surfaces. A corrolary effect consisted of a dedifferentiation of the topographic organization of the cortical maps representing these surfaces (**Figure 1**). However, this somatotopy disruption was relatively less pronounced for the representation of ipsilesional hindpaw, consistently with the contralateral predominance of vestibulo-thalamic projections [46, 47] (cat). The rapid deafferentation-induced expansion of cutaneous receptive field indicates that in intact animals, vestibular inputs exert a suppressive effect onto synaptic inputs driving cutaneous responses in S1.

It is well documented that cortical maps are dynamically reshaped through ongoing adjustments in the balance of excitatory and inhibitory influences on their constituent neurons. Hence, it is very likely that the receptive field enlargement induced by the vestibular loss results from a disinhibition process, possibly via thalamo-cortical inputs on S1 inhibitory interneurons or direct cortico-cortical connections*.* It has long been argued that intracortical inhibition plays a key role in controlling the spatial selectivity of cortical neurons through segregation of broad sets of converging synaptic inputs. Consistently, studies have reported a substantial enlargement of the cutaneous receptive field of somatosensory cortical neurons when GABA-mediated local inhibition was antagonized by an intracortical bicuculine injection [48–50] (cat; racoon), whereas injection of baclofen, a selective agonist for the GABAA receptors, induced a shrinkage of these receptive fields [51] (rat). A release of afferent-driven intracortical tonic inhibition results in an enhanced effectiveness of convergent cutaneous inputs. Therefore, this could be a most likely mechanism for rapid unmasking of previously subthreshold afferent connections reflected by the rapid expansion of cutaneous receptive field of S1 neurons following the loss of vestibular inputs. Our results extend previous findings, already mentioned in the present review, showing that auditory inputs to V1 decrease visually induced activity (mouse), while acute hearing loss releases the inhibitory effects of A1 neurons on visually elicited responses in V1 and leads to a concomitant increase in V1 activation [52] (mouse). As also previously noted, auditory stimulation sharpens the orientation selectivity of V1 neurons [22] (mouse). Collectively, the available evidence supports the view that, in normal conditions, cross modal modulation between primary cortical cortices may act to improve the tuning of neuronal response properties in these areas. In our study, the postlesion expansion of cutaneous RF was selectively located on the hindpaw plantar skin surfaces. Hence, we hypothesize that, in normal conditions, the vestibular influences on the S1 cortex could improve tactile acuity during perceptually guided posturo-locomotor adjustments.
