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

Resting state spinal fMRI will be useful in studies of normal spinal cord function and central nervous system disorders.

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.

During axolotl spinal cord regeneration adult neural stem cells reactivate an embryonic neuroepithelial cell-like gene program that implements planar cell polarity to orient cell divisions, coupling polarized spinal cord growth with stem cell self-renewal.

A genetically-defined population of spinal interneurons is reciprocally connected with spinal locomotor circuits and mediates recovery of locomotor function following spinal cord transection.

A signal amplifier network that transmits mechanical pain is delineated through characterising an excitatory interneuron population in the spinal cord dorsal horn and defining the postsynaptic populations they regulate.

Integrating decades of small-scale experiments with human gene expression data provides a systems-level view of the coordinated molecular processes triggered by spinal cord injury, and their relationship to recovery.

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