Extrinsic inhibitors in axon sprouting and functional recovery after spinal cord injury

Recovery from CNS injury is limited because CNS axons fail to grow after injury. There are two types of axonal growth: regeneration (growth from injured neurons) and sprouting (growth from uninjured neurons). Inhibitory molecules and a lack of growth-promoting factors restrict axon growth after injury. Manipulating extrinsic inhibitors alters the axonal sprouting response of intact axons. Promoting uninjured axon sprouting may be an alternative approach to improve recovery from spinal cord injury. This mini-review evaluates the evidence that modulation of extrinsic inhibitors of axon growth can increase sprouting of uninjured axons, which can mediate functional recovery from spinal cord injury.

• 1
  Inhibition of Nogo signaling leads to axon sprouting after spinal cord injury. Administration of an antibody that recognizes Nogo-A increased sprouting of the intact CST and functional recovery.
• 2
  Genetic deletion of PlexinA2 leads to increased sprouting of the intact CST on both sides of the cervical spinal cord after pyramidotomy, as well as increased functional recovery.
• 3
  ChABC treatment has been shown to increase CST sprouting and functional recovery of paw preference for weight support during rearing.