Recovery from spinal cord injury mediated by antibodies to neurite growth inhibitors

• Published in: Nature (London) Vol. 378; no. 6556; pp. 498 - 501
• Main Authors: Bregman, Barbara S, Kunkel-Bagden, Ellen, Schnell, Lisa, Dai, Hai Ning, Gao, Da, Schwab, Martin E
• Format: Journal Article
• Language: English
• Published: London Nature Publishing 30-11-1995; Nature Publishing Group
• Subjects: Animals; Axons - physiology; Biological and medical sciences; Brain Stem - cytology; Cell Division; Cellular biology; Central nervous system; Development. Senescence. Regeneration. Transplantation; Fundamental and applied biological sciences. Psychology; Growth Inhibitors - antagonists & inhibitors; Growth Inhibitors - immunology; Inhibitors; Locomotion; Nerve Regeneration; Neural Pathways; Neuronal Plasticity; Plasticity; Rats; Rats, Inbred Lew; Reflex; Regrowth; Rodents; Spinal cord injuries; Spinal Injuries - therapy; Vertebrates: nervous system and sense organs; Growth inhibitor; Spinal cord; Neurite; Rat; Antibody; Growth; Rodentia; Central nervous system; Regeneration; Vertebrata; Mammalia; Plasticity; Lesion
• ISSN: 0028-0836; 1476-4687
• DOI: 10.1038/378498a0

There is little axonal growth after central nervous system (CNS) injury in adult mammals. The administration of antibodies (IN-1) to neutralize the myelin-associated neurite growth inhibitory proteins leads to long-distance regrowth of a proportion of CNS axons after injury. Our aim was: to determine if spinal cord lesion in adult rats, followed by treatment with antibodies to neurite growth inhibitors, can lead to regeneration and anatomical plasticity of other spinally projecting pathways; to determine if the anatomical projections persist at long survival intervals; and to determine whether this fibre growth is associated with recovery of function. We report here that brain stem-spinal as well as corticospinal axons undergo regeneration and anatomical plasticity after application of IN-1 antibodies. There is a recovery of specific reflex and locomotor functions after spinal cord injury in these adult rats. Removal of the sensorimotor cortex in IN-1-treated rats 2-3 months later abolished the recovered contact-placing responses, suggesting that the recovery was dependent upon the regrowth of these pathways.