A new method was developed for the clinical assessment of motor function in rats after experimental spinal cord injury. The method consists of placing the animal on an inclined plane which can be adjusted to provide a slope of varying grade, and then assessing the maximum angle of the plane at which the animal can maintain its position without falling. The method was used to quantitate motor function in normal rats and in rats subjected to myelectomy, and consistently showed major differences between the two groups. The method has many positive features: the plane is easy to construct and of low cost; and the test is rapid, non-invasive, repeatable, and consistent.
Spinal cord blood flow (SCBF) was measured in 12 albino rats following acute cord injury produced by the extradural clip compression technique. Severe injury was produced with the clip compressing the cord with a force of 180 gm for 5 minutes, an injury previously shown to produce a severe functional deficit. Regional SCBF was measured 15 minutes, 2 hours, and 24 hours after injury by the 14C-antipyrine autoradiographic technique and a scanning microscope photometer. At 15 minutes and 2 hours, white and gray matter blood flow was severely diminished, and, at 24 hours, there was only minimal improvement. Focal decreases in blood flow were seen in white and gray matter for a considerable distance proximal and distal to the site of cord trauma. Thus, it has been confirmed in this model that severe cord compression injury produces severe posttraumatic ischemia in the cord which lasts for at least 24 hours.
The effect of papaverine, nitroprusside, or myelotomy on the recovery of spinal cord function was studied in rats after acute cord-compression injury. Spinal cord recovery was measured by a quantitative method of clinical assessment previously developed in our laboratory. Neither papaverine nor nitroprusside improved recovery of cord function. Dorsal midline myelotomy extending anteriorly as far as the central canal did not produce significant improvement (p greater than 0.05). However, when the myelotomy extended completely through the cord in the anteroposterior plane significant improvement (p less than 0.01) was obtained.
The concentration of axons in the pyramidal tract of normal and spinal cord-injured rats was determined by counting axons in sections of spinal cord stained by the Holmes technique. In the normal rat the axon concentration was uniform in the cervical, thoracic, and lumbar regions, although the size of the tract diminished progressively with its descent in the cord. After acute cord transection or compression injury, the axon concentration distal to the injury site diminished markedly. However, an appreciable number of distal axons persisted after injury, due to either delayed degeneration or to the presence of an admixture of afferent fibers. The axonal counting technique developed in this study should be helpful in experiments on spinal cord injury and regeneration.
Studies were performed on the effect of triiodo-L-thyronine (T3) on clinical recovery and axonal counts in the pyramidal tract of 56 rats subjected to an acute spinal cord compression injury at T-7. The T3 was given at a daily dose of 5 micrograms/kg for 4 weeks to 28 rats in the treatment group. The treatment and control animals were tested weekly for clinical recovery, and cord function as determined by the inclined-plane technique. Groups of animals were killed at 4 weeks and 12 weeks, and the axons in the pyramidal tract cephalad and caudad to the injury site were counted in sections prepared with Holmes' silver stain. There was no difference in clinical recovery between the treatment and control groups. This negative result contrasts with other studies which showed improved recovery of cord-injured animals treated with thyroid hormones. The possible explanations for this discrepancy are discussed. Similarly, there was no difference in the axon counts between the treated and control groups. Thus, T3 did not improve recovery or axonal regeneration in the pyramidal tract of rats after acute spinal cord compression injury. Between 4 and 12 weeks, there was a marked reduction in the cephalad axon counts in the pyramidal tract in both groups, indicating that approximately 50% of the axons in the pyramidal tract had undergone retrograde degeneration or dying back by 12 weeks after this degree of injury. The T3 did not affect the degree of retrograde degeneration.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.