In the injured sciatic nerve, blood-derived monocytes and macrophages eat dying leukocytes, thereby contributing to nerve debridement and inflammation resolution, and this correlates with neuronal regeneration.

Retrograde transport of NT-3 stimulated the reorganization of lumbar neural circuitry and synaptic connectivity remote to a thoracic SCI, along with improved behavioral recovery.

Two seemingly distinct cellular stress response pathways that contribute to neurodegeneration after axonal insults are now revealed to be under the control of a single master regulator of the neuronal injury response, the kinase DLK.

An interdisciplinary approach uncovers a new antinociceptive molecular mechanism and shows that the adhesion GPCR CIRL adjusts the sensation of gentle touch and noxious mechanical insult in opposite directions.

Localized drug photoactivation provides light-mediated analgesia in behaving mice.

Cell-specific alternative splicing of the synaptic calcium channel gene Cacna1b is controlled by exon hypomethylation and CTCF binding and is disrupted following nerve injury.

The DLK response pathway in neurons initiates the cascade of events leading to neuropathic pain after injury.

Competition between adhesive and tensile forces regulates axon fasciculation, thus introducing a new role of mechanical tension in the development of neural networks.

In vivo experiments on transgenic mice, and cell culture studies, establish Schwann cell c-Jun as a central regulator of peripheral nerve repair, and repair failure, during aging and chronic denervation.

Distinctive microenvironments within demyelinated white matter determine fate decisions of adult oligodendrocyte progenitor cells.