Abstract
Despite the robust regenerative potential of the peripheral nervous system, a permanent loss of function is often associated with injury. A multitude of causes have been implicated in this outcome, including the presence of a non-permissive microenvironment surrounding the injury and the regrowth of emerging neurites towards inappropriate targets. Preferential motor reinnervation is a naturally occurring phenomenon where motor axons have increased accuracy in reaching their appropriate end targets as the course of regeneration proceeds1. Several molecules have been implicated in encouraging this response, including two carbohydrates — Polysialic Acid (PSA) and Human Natural Killer Epitope-1 (HNK-1)2,3. Peptide mimics of these molecules have been identified4,5, which are more stable and economical than their glycan counterparts, and have independently been shown to enhance PMR in a soluble form, but only for transection distances substantially smaller than the 5-mm ‘critical gap’ size for mice6,7.