Paired Immunoglobulin-like Receptor B Knockout Does Not Enhance Axonal Regeneration or Locomotor Recovery after Spinal Cord Injury

Myelin components inhibit axonal regeneration in the central nervous system. This study investigates whether removing the Paired Immunoglobulin-like Receptor B (PIR-B), a receptor that interacts with myelin inhibitors, can enhance axonal regeneration after spinal cord injury. The researchers assessed corticospinal tract (CST) regeneration in PIR-B-knock-out mice and found that hindlimb motor function did not differ significantly between PIR-B-knock-out and wild-type mice after spinal cord injury. The results suggest that PIR-B knock-out alone is not enough to induce significant axonal regeneration after spinal cord injury, indicating other factors or signals may be involved in inhibiting axonal regeneration.

• 1
  Hindlimb motor function, assessed using various tests, did not significantly differ between PIR-B-knock-out and wild-type mice after dorsal hemisection of the spinal cord.
• 2
  Tracing of CST fibers after injury did not reveal enhanced axonal regeneration or sprouting in the CST of the PIR-B-knock-out mice.
• 3
  Systemic administration of NEP1–40, a NgR antagonist, to PIR-B knock-out mice did not enhance the regenerative response.