Wallerian degeneration: Gaining perspective on inflammatory events after peripheral nerve injury

Peripheral nerve injury (PNI) can lead to nerve gaps that hinder axon regrowth, and the supportive environment for PNS axons is not sustained. Studying PNI could inform improvements in PNS regeneration and recovery after CNS injury. The inflammatory response after PNI begins with axonal disintegration, causing blood-nerve barrier permeabilization and activating Schwann cells and resident macrophages. These cells then clear debris and promote axon regeneration. Unlike the CNS, the PNS inflammatory response is transient and efficient. In contrast, CNS inflammation can lead to inhibitory scar formation and cell degeneration.

• 1
  Axon degeneration in the distal nerve instigates subsequent degenerative processes after PNI; however, axon degeneration does not begin immediately.
• 2
  Schwann cells, the ensheathing glial cells of the PNS, are crucial for normal nerve function and for nerve repair, providing trophic support and producing basal lamina that supports axonal growth.
• 3
  Hematogenous macrophages are essential for effective myelin phagocytosis and produce cytokines that activate Schwann cells and trophic factors that aid axon regeneration.