Beta-aminopropionitrile treatment can accelerate recovery of mice after spinal cord injury.
Modulations of the extracellular matrix and scar formation following central nervous system (CNS) injuries are considered prohibitive for axon regeneration, thus restricting functional recovery. Recent findings indicating that lysyl oxidase, an extracellular matrix-forming enzyme, appears in a time-dependent manner at brain injury sites have suggested that inhibition of this enzyme may be conducive for regeneration and functional recovery. Here, we report that after unilateral spinal cord transection in adult mice, daily treatment (for 20 days) with the lysyl oxidase inhibitor beta-aminopropionitrile (100 mg/kg intraperitoneal) resulted in accelerated and more complete functional recovery. The mode of functional recovery, however, indicates that axonal regeneration of long descending tracts did not occur.
Gilad
G M
GM
Research and Development, Laboratory of Neuroscience, Assaf Harofeh Medical Center, P.O. Beer Yaakov, Zrifin 70300, Israel. gmgilad@asaf.health.gov.il
Gilad
V H
VH
D000629:Aminopropionitrile / Q000627:therapeutic use*; D000818:Animals; D004791:Enzyme Inhibitors / Q000627:therapeutic use; D006614:Hindlimb / Q000503:physiopathology; D008124:Locomotion / Q000187:drug effects; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008249:Protein-Lysine 6-Oxidase / Q000037:antagonists & inhibitors*; D013119:Spinal Cord Injuries / Q000188:drug therapy* / Q000503:physiopathology; D013997:Time Factors
D004791:Enzyme Inhibitors; D000629:Aminopropionitrile; D008249:Protein-Lysine 6-Oxidase