Sensory afferents regenerated into dorsal columns after spinal cord injury remain in a chronic pathophysiological state

Exp Neurol. 2007 Aug;206(2):257-68. doi: 10.1016/j.expneurol.2007.05.013. Epub 2007 May 23.


Axon regeneration after experimental spinal cord injury (SCI) can be promoted by combinatorial treatments that increase the intrinsic growth capacity of the damaged neurons and reduce environmental factors that inhibit axon growth. A prior peripheral nerve conditioning lesion is a well-established means of increasing the intrinsic growth state of sensory neurons whose axons project within the dorsal columns of the spinal cord. Combining such a prior peripheral nerve conditioning lesion with the infusion of antibodies that neutralize the growth inhibitory effects of the NG2 chondroitin sulfate proteoglycan promotes sensory axon growth through the glial scar and into the white matter of the dorsal columns. The physiological properties of these regenerated axons, particularly in the chronic SCI phase, have not been established. Here we examined the functional status of regenerated sensory afferents in the dorsal columns after SCI. Six months post-injury, we located and electrically mapped functional sensory axons that had regenerated beyond the injury site. The regenerated axons had reduced conduction velocity, decreased frequency-following ability, and increasing latency to repetitive stimuli. Many of the axons that had regenerated into the dorsal columns rostral to the injury site were chronically demyelinated. These results demonstrate that regenerated sensory axons remain in a chronic pathophysiological state and emphasize the need to restore normal conduction properties to regenerated axons after spinal cord injury.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Action Potentials / drug effects
  • Action Potentials / physiology
  • Afferent Pathways / pathology
  • Afferent Pathways / physiopathology*
  • Animals
  • Antibodies / immunology
  • Antibodies / pharmacology
  • Antibodies / therapeutic use
  • Antigens / immunology
  • Axons / pathology*
  • Cicatrix / drug therapy
  • Cicatrix / immunology
  • Cicatrix / prevention & control
  • Electric Stimulation
  • Gliosis / drug therapy
  • Gliosis / immunology
  • Gliosis / prevention & control
  • Growth Inhibitors / antagonists & inhibitors
  • Growth Inhibitors / immunology
  • Nerve Fibers, Myelinated / drug effects
  • Nerve Fibers, Myelinated / immunology
  • Nerve Fibers, Myelinated / pathology
  • Nerve Regeneration*
  • Neural Conduction / drug effects
  • Neural Conduction / physiology
  • Neurons, Afferent* / pathology
  • Peripheral Nerves / drug effects
  • Peripheral Nerves / immunology
  • Peripheral Nerves / physiopathology
  • Proteoglycans / antagonists & inhibitors
  • Proteoglycans / immunology
  • Rats
  • Rats, Sprague-Dawley
  • Reaction Time / drug effects
  • Reaction Time / physiology
  • Spinal Cord Injuries / pathology
  • Spinal Cord Injuries / physiopathology*


  • Antibodies
  • Antigens
  • Growth Inhibitors
  • Proteoglycans
  • chondroitin sulfate proteoglycan 4