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Restoring locomotion after complete spinal cord injury does not require locomotor training, only the return of sufficient excitability within neurons of the spinal cord.

Calpain is a promising therapeutic target to reduce spasticity after a spinal cord injury.

Members of the BMP family of growth factors act as a reiterative code of distinct activities to direct the identities of different classes of sensory neurons in the spinal cord.

Unlike in early embryonic development, injured spinal cord and muscle in Xenopus laevis larvae recruit non-canonical Hedgehog signaling essential for their regeneration, while repressing Gli transcriptional activity.

Conditional silencing of long ascending propriospinal neurons disrupts interlimb coordination of the fore and hindlimb pairs, but in a highly context-specific manner.

Identification of a novel role for central nervous system-resident progenitors in the patterning of the vascular network around the developing spinal cord.

Genetic analyses combining photoconvertible cell signalling reporters with gain- and loss-of function manipulations reveal a novel role for Notch signalling in controlling Hedgehog response in neural progenitor cells.

Myelin-associated inhibitors and chondroitin sulfate proteoglycans are not the primary mechanism stopping sensory axons regenerating into the spinal cord, although their removal can markedly enhance regeneration when combined with an intervention that elevates axon growth capacity sufficiently robustly.

Precisely-timed bursts of closed-loop vagus nerve stimulation during rehabilitation restore neural connectivity and substantially improve recovery of motor function after SCI.

Motor exit point (MEP) glia utilize mechanisms most commonly attributed to neural crest cells for their development from spinal cord precursors.