Treadmill running protects spinal cord contusion from secondary degeneration.
It is known that physical activity triggers changes in the central nervous system. Adult rats, trained on treadmills for 4 weeks, and a group of sedentary rats was submitted to contuse moderate spinal cord injury. A group of sedentary rats was submitted to a sham operation. The trained group continued running on treadmill after lesion for 4 weeks. Motor behavior evaluated by BBB score was smaller in the sedentary group compared to the trained rats by 7 days after lesion. Computerized activity monitor showed clear-cut differences in spontaneous motor parameters in trained rats only before lesion. After surgery, sedentary rats showed changes in motor parameters but not in later periods of analysis. Animals were euthanized by 28 days after surgery, and their spinal cords were processed for Nissl staining and immunohistochemistry. The number of the remaining neurons and the lesion areal and lesion volume fractions were obtained by stereological method. The number of the remaining neurons did not change after training. Lesion volume and lesion areal fraction per section were smaller in the trained group. Lesion index was more pronounced in the sedentary group. Microdensitometric image analysis demonstrated a microglial reaction, astroglial activation, and glial FGF-2 production more pronounced in the spinal cord of sedentary animals. GAP-43 was higher in caudal levels of contusion in the sedentary group. In conclusion, treadmill running may favor a better functional recovery in the acute period after spinal cord lesion and wound repair processes leading to neuroprotection.
Andrade
Michele Schultz Ramos
MS
Neuroregeneration Center, Experimental Neurology Division, Department of Neurology, University of São Paulo School of Medicine, Av. Dr. Arnaldo, 455, CEP: 01246-903, São Paulo, Brazil.
Mendonça
Lúcio Mário
LM
Chadi
Gerson
G
D000818:Animals; D039481:CD11b Antigen / Q000378:metabolism; D002452:Cell Count; D016222:Fibroblast Growth Factor 2 / Q000378:metabolism; D019922:GAP-43 Protein / Q000378:metabolism; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007091:Image Processing, Computer-Assisted; D007150:Immunohistochemistry; D008297:Male; D009043:Motor Activity / Q000502:physiology; D009410:Nerve Degeneration / Q000209:etiology / Q000473:pathology*; D009457:Neuroglia / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D013119:Spinal Cord Injuries / Q000150:complications / Q000473:pathology*
D039481:CD11b Antigen; D019922:GAP-43 Protein; D005904:Glial Fibrillary Acidic Protein; D016222:Fibroblast Growth Factor 2