Neuroscience
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Brain injuries such as focal stroke initiate a myriad of neural events leading to local and remote alterations in cerebral networks. The neurochemical and neurophysiological mechanisms underlying these postlesion changes raise the question of their beneficial or adverse effects on functional recovery. In this review, we aim to reconcile findings from animal and patients studies using a "from cellular-to network-levels" perspective to gain further insights into the neuroplasticity mechanisms underlying recovery of sensorimotor functions. Ultimately, an integrative view of the multiple facets of poststroke changes should give an impetus to novel neurorehabilitation strategies by providing evidence of how neuroscience findings can be translated and operationalized within the context of restorative stroke.
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The adult brain retains a considerable capacity to functionally reorganize its circuits, which mainly relies on the prevalence of three basic processes that confer plastic potential: synaptic plasticity, plastic changes in intrinsic excitability and, in certain central nervous system (CNS) regions, also neurogenesis. Experimental models of peripheral nerve injury have provided a useful paradigm for studying injury-induced mechanisms of central plasticity. In particular, axotomy of somatic motoneurons triggers a robust retrograde reaction in the CNS, characterized by the expression of plastic changes affecting motoneurons, their synaptic inputs and surrounding glia. ⋯ Our group has identified the highly reactive gas nitric oxide (NO) as one of these signals, by providing robust evidence for its key role to induce synapse elimination and increases in intrinsic excitability following motor axon damage. We have elucidated operational principles of the NO-triggered downstream transduction pathways mediating each of these changes. Our findings further demonstrate that de novo NO synthesis is not only "necessary" but also "sufficient" to promote the expression of at least some of the features that reflect reversion toward a dedifferentiated state in axotomized adult motoneurons.
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One of the most striking demonstrations of experience-dependent plasticity comes from studies of sensory-deprived individuals (e.g., blind or deaf), showing that brain regions deprived of their natural inputs change their sensory tuning to support the processing of inputs coming from the spared senses. These mechanisms of crossmodal plasticity have been traditionally conceptualized as having a double-edged sword effect on behavior. On one side, crossmodal plasticity is conceived as adaptive for the development of enhanced behavioral skills in the remaining senses of early-deaf or blind individuals. ⋯ In the present review we stress that this dichotomic vision is oversimplified and we emphasize that the notions of the unavoidable adaptive/maladaptive effects of crossmodal reorganization for sensory compensation/restoration may actually be misleading. For this purpose we critically review the findings from the blind and deaf literatures, highlighting the complementary nature of these two fields of research. The integrated framework we propose here has the potential to impact on the way rehabilitation programs for sensory recovery are carried out, with the promising prospect of eventually improving their final outcomes.
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Loudness is the primary perceptual correlate of sound intensity. The relationship between sound intensity and loudness is not fixed, and can be modified by short-term sound deprivation or stimulation. ⋯ Although there is sufficient evidence to conclude that loudness can be modulated in normal hearing listeners by temporary sound deprivation and stimulation, evidence is scanter for the hearing-impaired listeners. In addition, cortical effects of sound deprivation and stimulation in humans, which may correlate with loudness coding, are still largely unknown and should be the target of future research.
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Multiple sclerosis (MS) is a chronic neurological disease characterized by inflammation and degeneration within the CNS. Over the course of the disease, most MS patients successively accumulate inflammatory lesions, axonal damage, and a rather diffuse CNS pathology, along with an increasing degree of disability. Pharmacological treatment options which are currently approved for MS aim at limiting inflammation and decreasing the relapse rate, or at simply relieving symptoms. ⋯ In addition, and probably closest to rehabilitative approaches, practice-induced plasticity has been probed in a few studies. Altogether, there is growing evidence for a preservation of rapid-onset motor plasticity and for functionally relevant chronic reorganization processes, which might be limited by high CNS injury in advanced stages of the disease. Clinical implications of these findings with regard to the development and optimization of rehabilitative treatments in MS are discussed, as well as open questions which need to be addressed by future studies.