title: The role of GM1-ganglioside in the injured spinal cord of rats: an immunohistochemical study using GM1-antisera.
abstract: The effect of GM1-ganglioside (GM1) administration was investigated in the injured spinal cord of rats. Immunohistochemistry using GM1-antisera was applied in the study of GM1 distribution, and locomotor recovery was also evaluated. A total of 86 rats, subdivided into four groups, were used in the study. The SI + GM1 group (n = 30) underwent a thoracic cord injury, and then received daily intraperitoneal injections of GM1 (10 mg/kg) from 0 to 13 days after injury. The SI group (n = 30) also underwent thoracic cord injury, but did not receive GM1 treatment. The GM1 group (n = 20) received daily injections of GM1 in the absence of any spinal cord injury. The control group (n = 6) neither underwent spinal cord injury nor received GM1 treatment. The animals were sacrificed at 1, 3, 5, 7, and 14 days after injury for immunohistochemical evaluation. GM1 immunoreactive axons, myelin sheaths, and glial cells were counted in 5 light microscopic fields of spinal white matter. Immunohistochemical studies of the spinal cord revealed that GM1 treatment significantly increased both GM1-positive axons and GM1-positive myelin sheaths in the lateral funiculus surrounding the lesion site. The exogenous GM1 was incorporated predominantly into the myelin sheath rather than the axon. This distribution was detectable by day 1 of injury and persisted until day 14, and was significantly different from that of the control group on days 1 and 7. Moreover, GM1 treatment significantly accelerated the recovery of motor function. Collectively, these results suggest that exogenous GM1 administration after a spinal cord injury results in the rapid transfer of GM1 to the lateral funiculus where the motor transmission pathway is located. Furthermore, exogenous GM1 was shown to be specifically incorporated into the myelin sheath. Thus GM1 treatment may prevent demyelination and may contribute to motor function recovery.
authors.affiliation: Department of Orthopedic Surgery, Shiga University of Medical Science, Otsu, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Imanaka
authors.forename: S
authors.initials: S
authors.lastname: Hukuda
authors.forename: T
authors.initials: T
authors.lastname: Maeda
mesh_terms: D000818:Animals; D001369:Axons / Q000648:ultrastructure; D002452:Cell Count / Q000187:drug effects; D005732:Gangliosides / Q000494:pharmacology*; D007106:Immune Sera / Q000494:pharmacology*; D007150:Immunohistochemistry; D008297:Male; D009043:Motor Activity / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D013119:Spinal Cord Injuries / Q000188:drug therapy*
chemical_list: D005732:Gangliosides; D007106:Immune Sera