3-nitrotyrosine and Radiculopathy

Experimental animal study.. This study investigated whether nitric oxide (NO) mediated protein nitration is involved in the pathogenesis of radiculopathy and whether the symptoms can be relieved by its suppression.. It has been reported that nitration of protein mediated by NO is involved in the degenerative neurological disorders, but its involvement is not clear in the radiculopathy.. Two kinds of rat models of radiculopathy were used. Radiculopathy was induced either by ligation of spinal nerve roots or transplantation of autologous nucleus pulposus. In separate groups of rats, aminoguanidine, a potent nitric oxide synthetase inhibitor, was administered just before induction of radiculopathy, to suppress NO production and resultant nitration of protein. Sensation of the hind limb was evaluated by plantar stimulation test, and motor weakness was assessed by observation of gait pattern. Nitrotyrosine, product of protein nitration, was assayed quantitatively by Western immunoblotting.. Mechanical allodynia was observed in both compression and nucleus pulposus groups, but motor weakness was observed only in the compression group. Preoperative administration of aminoguanidine attenuated mechanical allodynia and motor weakness. Optical densities of nitrotyrosine bands increased significantly in radiculopathy groups, but they were lowered by administration of aminoguanidine.. NO mediated protein nitration contributes to the development of both types of radiculopathies. Suppression of NO production can decrease protein nitration and relieve neural dysfunctions of radiculopathy.. N/A.

Topics: Animals; Blotting, Western; Disease Models, Animal; Enzyme Inhibitors; Guanidines; Hindlimb; Hyperalgesia; Intervertebral Disc; Ligation; Nitric Oxide; Nitric Oxide Synthase; Proteins; Radiculopathy; Rats; Rats, Sprague-Dawley; Spinal Nerve Roots; Transplantation, Autologous; Tyrosine

This study was conducted to investigate the electromyographic changes and their pathophysiologic background in the animal model of nucleus pulposus-induced radiculopathy.. To observe the abnormal spontaneous activities in the electromyography (EMG) of rats with nucleus pulposus-induced radiculopathy and assess the role of nitric oxide in their development.. It has been shown that application of nucleus pulposus to nerve roots induces changes consistent with radiculopathy. However, to our knowledge, electromyographic findings and their background have never been studied in this model of radiculopathy.. Autologous nucleus pulposus was harvested from the tails of Sprague-Dawley rats, and applied to L4 and L5 nerve roots. The rats were tested for mechanical allodynia, motor paresis, and needle EMG, before and after surgery. Specimens of nerve roots were stained histochemically for nitrotyrosine.. The rats had mechanical allodynia after surgery, but motor paresis was absent. EMG showed abnormal spontaneous activities after surgery, but only temporarily. Immunoreactivity for nitrotyrosine was detected in the cell bodies and axons of nerve roots.. The data indicate that abnormal spontaneous activities can be observed in electromyographic examination of nucleus pulposus-induced radiculopathy. The development of these activities is considered related to nitric oxide-mediated protein nitration and resultant axonal dysfunction.

Topics: Animals; Disease Models, Animal; Electromyography; Fluorescent Antibody Technique, Indirect; Ganglia, Spinal; Hyperalgesia; Immunoenzyme Techniques; Intervertebral Disc; Male; Muscle, Skeletal; Paresis; Radiculopathy; Rats; Rats, Sprague-Dawley; Spinal Nerve Roots; Tyrosine