Neuroplasticity Research

KEY FINDING: Total density of dendritic spines on lamina II neurons did not change after spinal cord injury.

KEY FINDING: Synaptic inputs from individual regenerated axons also matched the properties in unlesioned animals, although this was associated with changes in release parameters.

KEY FINDING: Active regeneration of nerve gaps through the conduit was confirmed from 10 days onwards, with varied GAP-43 expression throughout the regeneration tissue.

KEY FINDING: Genetic deletion of RhoA and RhoC suppresses axon retraction or dieback after spinal cord injury.

KEY FINDING: Locomotor training can improve functional locomotor abilities by exploiting the neuronal plasticity of the spinal cord, reinforcing appropriate connections in an activity-dependent manner.

KEY FINDING: PKCγ is activated in the corticospinal tract (CST) on the uninjured side of the brain after TBI, suggesting it plays a role in the brain's response to injury.

KEY FINDING: NgR1 regulates the distribution of Caspr, a paranodal protein, influencing the intramembranous cleavage of the protein at the junction. This finding correlated with altered ultrastructural organization at the paranode and internode of ngr1−/−mice.

KEY FINDING: Identified druggable targets to intervene with secondary brain injuries like ischemia, hemorrhage, and mitochondrial dysfunction after TBI.

KEY FINDING: Acute chondroitinase infusion decreased intact CSPGs and significantly increased pericontusional cortical grey and white matter GAP43-positive axon sprouting at 7 days post-injury.

KEY FINDING: Spinal cord injury leads to changes in the motor cortex, with increased activity in both existing and new areas of the brain.