Functional electrical stimulation helps replenish progenitor cells in the injured spinal cord of adult rats.
Functional electrical stimulation (FES) can restore control and offset atrophy to muscles after neurological injury. However, FES has not been considered as a method for enhancing CNS regeneration. This paper demonstrates that FES dramatically enhanced progenitor cell birth in the spinal cord of rats with a chronic spinal cord injury (SCI). A complete SCI at thoracic level 8/9 was performed on 12 rats. Three weeks later, a FES device to stimulate hindlimb movement was implanted into these rats. Twelve identically-injured rats received inactive FES implants. An additional control group of uninjured rats were also examined. Ten days after FES implantation, dividing cells were marked with bromodeoxyuridine (BrdU). The "cell birth" subgroup (half the animals in each group) was sacrificed immediately after completion of BrdU administration, and the "cell survival" subgroup was sacrificed 7 days later. In the injured "cell birth" subgroup, FES induced an 82-86% increase in cell birth in the lumbar spinal cord. In the injured "cell survival" subgroup, the increased lumbar newborn cell counts persisted. FES doubled the proportion of the newly-born cells which expressed nestin and other markers suggestive of tripotential progenitors. In uninjured rats, FES had no effect on cell birth/survival. This report suggests that controlled electrical activation of the CNS may enhance spontaneous regeneration after neurological injuries.
Becker
Daniel
D
International Center, for Spinal Cord Injury, Hugo Moser Research Institute, Department of Neurology, Johns Hopkins School of Medicine and Kennedy Krieger Institute, Baltimore, MD 21205, USA.
Gary
Devin S
DS
Rosenzweig
Ephron S
ES
Grill
Warren M
WM
McDonald
John W
JW
D053687:Adult Stem Cells / Q000502:physiology*; D000704:Analysis of Variance; D000818:Animals; D000941:Antigens / Q000378:metabolism; D001703:Biophysics / Q000379:methods; D001973:Bromodeoxyuridine / Q000378:metabolism; D039481:CD11b Antigen / Q000378:metabolism; D002470:Cell Survival; D004195:Disease Models, Animal; D004558:Electric Stimulation / Q000379:methods*; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D055495:Neurogenesis / Q000502:physiology*; D010751:Phosphopyruvate Hydratase / Q000378:metabolism; D011509:Proteoglycans / Q000378:metabolism; D051381:Rats; D020318:Rats, Long-Evans; D013119:Spinal Cord Injuries / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D000099216:Chondroitin Sulfate Proteoglycan 4
D000941:Antigens; D001973:Bromodeoxyuridine; D039481:CD11b Antigen; D005904:Glial Fibrillary Acidic Protein; D010751:Phosphopyruvate Hydratase; D011509:Proteoglycans; D000099216:Chondroitin Sulfate Proteoglycan 4