Alteration in axial motoneuronal morphology in the spinal cord injured spastic rat.
Following spinal cord injury (SCI), exaggerated reflexes and muscle tone emerge that contribute to a general spastic syndrome in humans. At present, the underlying mechanisms involved with the development of spasticity following traumatic spinal cord injury, especially with regard to axial musculature, remains unclear. The purpose of the present study was to examine the temporal changes in sacrocaudal motoneuronal morphology following complete transection of the sacral spinal cord and to correlate these changes with the onset and progression of spasticity within the tail musculature. The spinal cords of rats were transected at the upper sacral (S(2)) level. Animals were behaviorally tested for the onset and progression of spasticity in the tail and at 1, 2, 4, or 12 weeks postinjury were sacrificed. At these time points, the animals demonstrated stage 1, 2, 3, or 4 spastic behavior, respectively. Sacrocaudal motoneurons innervating selected flexor muscles within the tail were retrogradely labeled with cholera toxin beta-subunit and neuronal morphology was analyzed using a combination of immunocytochemistry and standard microscopy. Initially over the first 2 weeks postinjury, a transient increase in the lengths of primary and secondary dendrites occurred. However, a progressive decrease in the overall number of dendritic branches was observed between 2 and 12 weeks postinjury, which parallels the time frame for the progressive increase in spastic behavior in the tail musculature. Following spinal cord injury, there is an alteration in the morphology of tail flexor motoneurons, which may be relevant to the development of spasticity within the tail.
Kitzman
Patrick
P
Department of Rehabilitation Science, The University of Kentucky, 126G Charles T. Wethington Building, 900 South Limestone Avenue, Lexington, KY 40536-0200, USA. phkitz1@uky.edu
D000818:Animals; D048430:Cell Shape / Q000502:physiology; D048429:Cell Size; D002772:Cholera Toxin; D003712:Dendrites / Q000473:pathology; D004195:Disease Models, Animal; D018450:Disease Progression; D005260:Female; D009046:Motor Neurons / Q000473:pathology*; D009128:Muscle Spasticity / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D018482:Muscle, Skeletal / Q000294:innervation / Q000503:physiopathology*; D009410:Nerve Degeneration / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013119:Spinal Cord Injuries / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D013997:Time Factors
D002772:Cholera Toxin