Myelin status and oligodendrocyte lineage cells over time after spinal cord injury: What do we know and what still needs to be unwrapped?

Spinal cord injury (SCI) can lead to motor, sensory, and autonomic impairments, partly due to the loss of oligodendrocytes and demyelination. This review discusses the processes of demyelination and remyelination after SCI, and how oligodendrocyte progenitor cells respond to spinal trauma. NG2 cells are distributed evenly throughout the brain and spinal cord, occupying nonoverlapping domains throughout the entire gray and white matter. Because they can replace oligodendrocytes, NG2 cells have come to be known as oligodendrocyte progenitor cells (OPCs), among other names. Myelin debris prevents oligodendrocyte differentiation (Kotter, 2006; Plemel, Manesh, Sparling, & Tetzlaff, 2013), therefore its presence in and around the injury site may hamper oligodendrocyte differentiation, especially within the SCI lesion cavity where OPCs accumulate but rarely differentiate into oligodendrocytes

• 1
  OPCs proliferate and differentiate into myelinating oligodendrocytes for months after SCI.
• 2
  The extent and chronicity of demyelination after SCI likely depends on multiple factors, such as location, severity of injury and duration of post-SCI compression.
• 3
  Factors like CNTF and FGF-2 continue to be elevated for at least 3 months post-injury, promoting oligodendrocyte formation and new myelin production.