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It has been long known that somatosensory deafferentation can produce a dramatic reorganization of the somatotopic map, characterized by the retraction of the deafferented body part representation followed by expansion of unaffected body part representations (Pons et al., 1991). Mechanisms driving this phenomenon are not clear, nor is it evident whether they occur within the cortex and/or at subcortical structures (Florence et al., 1998; Jones and Pons, 1998; Jain et al., 2000). The occurrence of anatomical alterations in the cortex after deafferentation (Florence et al., 1998), in addition to the notion that neocortex is a very plastic structure, led to the view that cortical reorganization of sensory maps after lesions is driven, at least in part, by cortical mechanisms. Recent work published by Kambi et al. (2014) contradicts this paradigm. In order to determine the extent to which different sites of somatosensory pathway potentially contribute to cortical plasticity, Kambi and colleagues lesioned the dorsal column in monkeys. They then mapped the hand representation in area 3b during inactivation of the cortical face region or the cuneate nucleus. They showed that transient inactivation of normal chin representation in area 3b did not affect the expanded chin representation, even in the vicinity of the former face/hand boundary. Surprisingly, inactivation of the cuneate nucleus completely abolished responses of the expanded chin representation. These results suggest that after lesions of the dorsal column, reorganization in area 3b is dependent on plastic alterations in the brainstem, and not in the cortex. In fact, cortical reorganization was probably mediated by growth of trigeminal axons into the cuneate nucleus, as previously shown by Jain et al. (2000). The apparent absence of corticocortical mechanisms driving cortical receptive field reorganization in these experiments is very intriguing. Simultaneous recordings from the normal chin and deafferented body representation of S1 demonstrated the expansion of the chin area in animals with dorsal column lesions (Kambi et al., 2014). Based on previous studies, it would be expected that this was due to new corticocortical connections, at least in the vicinity of the face/hand border. Moreover, large-scale sprouting of cortical connections following forelimb deafferentation has already been shown by Florence et al. (1998). This divergence in the results might be related to the type of deafferentation. In Kambi et al. (2014), animals underwent a lesion in the dorsal column, which only interrupts the ascending somatosensory information from the forelimb. Unlike amputees or individuals that suffered complete sectioning of the spinal cord, they could still move their forelimb and consequently, the motor representation of the forelimb was still present. Accordingly, Kambi et al. (2011) has shown that the forelimb motor representation in M1 is substantially preserved after lesion of the dorsal column. Perhaps this is the key difference between models in which cortical mechanisms do or do not contribute to the reorganization of cortical maps. The hand representation in area 3b receives inputs from M1 (Liao et al., 2013). This direct feedback, as well as indirect inputs from other cortical areas, may be a potential source to keep cortical hand region activated during forelimb movements even after lesions of the dorsal column. In this scenario, maintenance of activity by area 3b cortical inputs would preclude production of signals that induce corticocortical sprouting, and so maintain the segregation between face and hand regions. This would explain why large-scale sprouting in area 3b was observed by Florence et al. (1998), but apparently not by Kambi et al. (2014). In that study, animals had amputations and at some point, they lost the motor representation of the missing body part. Accordingly, in humans that have suffered complete spinal cord injury, the reorganization of the somatosensory cortex also results from growth of new lateral connections in the cortex (Henderson et al., 2011). It is possible that depending on the type of deafferentation, the mechanisms driving the functional reorganization in the cortex can be called into action at different levels of the somatosensory system. It would be interesting to explore this question by using the same experimental protocol as Kambi et al. (2014) in amputee animals. Additionally, injections of neurotracers could be done into the deafferented

Are the mechanisms driving somatosensory reorganization cortical or subcortical?