Experimental neurology
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Experimental neurology · May 2012
ReviewTreatments to restore respiratory function after spinal cord injury and their implications for regeneration, plasticity and adaptation.
Spinal cord injury (SCI) often leads to impaired breathing. In most cases, such severe respiratory complications lead to morbidity and death. ⋯ This review article will highlight experimental SCI resulting in compromised breathing, the various methods of restoring function after such injury, and some recent findings from our own laboratory. Additionally, it will discuss findings about motor and CNS respiratory plasticity and adaptation with potential clinical and translational implications.
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Experimental neurology · May 2012
ReviewCortical and subcortical compensatory mechanisms after spinal cord injury in monkeys.
This is a review of our investigations into the neuronal mechanisms of functional recovery after spinal cord injury (SCI) in a non-human primate model. In primates, the lateral corticospinal tract (l-CST) makes monosynaptic connections with spinal motoneurons. The existence of direct cortico-motoneuronal (CM) connections has been thought to be the basis of dexterous digit movements, such as precision gripping. ⋯ Such changes in cortical activity in M1 and PMv have been shown to accompany changes in the expressions of plasticity-related genes, such as GAP-43. Changes in the dynamic properties of neural circuits, both at the cortical and subcortical levels, are time-dependent. Multidisciplinary studies to clarify how the changes in the dynamic properties of individual components of the large-scaled networks are coordinated during recovery will help to develop effective therapeutic strategies to recovery from SCI.
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Experimental neurology · May 2012
ReviewTraining and anti-CSPG combination therapy for spinal cord injury.
Combining different therapies is a promising strategy to promote spinal cord repair, by targeting axon plasticity and functional circuit reconnectivity. In particular, digestion of chondroitin sulphate proteoglycans at the site of the injury by the activity of the bacterial enzyme chondrotinase ABC, together with the development of intensive task specific motor rehabilitation has shown synergistic effects to promote behavioural recovery. This review describes the mechanisms by which chondroitinase ABC and motor rehabilitation promote neural plasticity and we discuss their additive and independent effects on promoting behavioural recovery.