Serum response factor promotes axon regeneration following spinal cord transection injury

Studies have snown that serum response factor is beneficaial for axonar regeneration of peripheral herves.However,Its role after central nervous system injury remains unclear. In this study,we established a rat model of T9-T10 spinal cord transection injury.We found that the expression of serum response factor in injured spinal cord gray matter neurons gradually increased with time,reached its peak on the 7^(th) day,and then gradually decreased.To investigate the role of serum response factor,we used lentivirus vecto rs to ove rexpress and silence serum response factor in spinal cord tissue.We found that overexpression of serum response factor promoted motor function recovery in rats with spinal cord injury.Qualitative observation of biotinylated dextran amine anterograde tra cing showed that ove rexpression of serum response factor increased nerve fibers in the injured spinal co rd.Additionally,transmission electron microscopy showed that axon and myelin sheath morphology was restored.Silencing serum response factor had the opposite effects of ove rexpression.These findings suggest that serum response factor plays a role in the recovery of motor function after spinal cord injury.The underlying mechanism may be related to the regulation of axonal regeneration.

Glial scar size, inhibitor concentration, and growth of regenerating axons after spinal cord transection

A mathematical model has been formulated in accordance with cell chemotaxis and relevant experimental data. A three-dimensional lattice Boltzmann method was used for numerical simulation. The present study observed the effects of glial scar size and inhibitor concentration on regenerative axonal growth following spinal cord transection. The simulation test comprised two parts： （1） when release rates of growth inhibitor and promoter were constant, the effects of glial scar size on axonal growth rate were analyzed, and concentrations of inhibitor and promoters located at the moving growth cones were recorded. （2） When the glial scar size was constant, the effects of inhibitor and promoter release rates on axonal growth rate were analyzed, and inhibitor and promoter concentrations at the moving growth cones were recorded. Results demonstrated that （1） a larger glial scar and a higher release rate of inhibitor resulted in a reduced axonal growth rate. （2） The axonal growth rate depended on the ratio of inhibitor to promoter concentrations at the growth cones. When the average ratio was 〈 1.5, regenerating axons were able to grow and successfully contact target cells.

Brain-derived neurotrophic factor and neural plasticity in a rat model of spinal cord transection

The present study employed a rat model of T10 spinal cord transection. Western blot analyses revealed increased brain-dedved neurotrophic factor （BDNF） expression in spinal cord segments caudal to the transection site following injection of replication incompetent herpes simplex virus vector （HSV-BDNF） into the subarachnoid space. In addition, hindlimb locomotor functions were improved. In contrast, BDNF levels decreased following treatment with replication defective herpes simplex virus vector construct small interference BDNF （HSV-siBDNF）. Moreover, hindlimb locomotor functions gradually worsened. Compared with the replication incompetent herpes simplex virus vector control group, extracellular signal regulated kinasel/2 expression increased in the HSV-BDNF group on days 14 and 28 after spinal cord transection, but expression was reduced in the HSV-siBDNF group. These results suggested that BDNF plays an important role in neural plasticity via extracellular signal regulated kinasel/2 signaling pathway in a rat model of adult spina cord transection.

Feasibility of 3.0 T diffusion-weighted nuclear magnetic resonance imaging in the evaluation of functional recovery of rats with complete spinal cord injury

Diffusion tensor imaging is a sensitive way to reflect axonal necrosis and degeneration, glial cell regeneration and demyelination following spinal cord injury, and to display microstructure changes in the spinal cord in vivo. Diffusion tensor imaging technology is a sensitive method to diagnose spinal cord injury; fiber tractography visualizes the white matter fibers, and directly displays the structural integrity and resultant damage of the fiber bundle. At present, diffusion tensor imaging is restricted to brain examinations, and is rarely applied in the evaluation of spinal cord injury. This study aimed to explore the fractional anisotropy and apparent diffusion coefficient of diffusion tensor magnetic resonance imaging and the feasibility of diffusion tensor tractography in the evaluation of complete spinal cord injury in rats. The results showed that the average combined scores were obviously decreased after spinal cord transection in rats, and then began to increase over time. The fractional anisotropy scores after spinal cord transection in rats were significantly lower than those in normal rats （P 〈 0.05）; the apparent diffusion coefficient was significantly increased compared with the normal group （P 〈 0.05）. Following spinal cord transection, fractional anisotropy scores were negatively correlated with apparent diffusion coefficient values （r = -0.856, P 〈 0.01）, and positively correlated with the average combined scores （r = 0.943, P 〈 0.01）, while apparent diffusion coefficient values had a negative correlation with the average combined scores （r = -0.949, P 〈 0.01）. Experimental findings suggest that, as a non-invasive examination, diffusion tensor magnetic resonance imaging can provide qualita- tive and quantitative information about spinal cord injury. The fractional anisotropy score and apparent diffusion coefficient have a good correlation with the average combined scores, which reflect functional recovery after spinal cord injury.

Management of acute spinal cord injury:A summary of the evidence pertaining to the acute management,operative and non-operative management

Acute traumatic spinal cord injury is often a lifechanging and devastating event with considerable mortality and morbidity.Over half a million people suffer from traumatic spinal cord injury annually with the majority resulting from road traffic accidents or falls.The Individual,societal and economic costs are enormous.Initial recognition and treatment of acute traumatic spinal cord injury are crucial to limit secondary injury to the spinal cord and to provide patients with the best chance of some functional recovery.This article is an overview of the management of the acute traumatic spinal cord injury patient presenting to the emergency department.We review the initial assessment,criteria for imaging and clearing the spine,and evaluate the literature to determine the optimum timing of surgery and the role of non-surgical treatment in patients presenting with acute spinal cord injury.

Inhibition of ciliary neurotrophic factor in a rat model of transected spinal cord

Ciliary neurotrophic factor （CNTF） dramatically increases following spinal cord injury and participates in the repair process, although some studies have shown that CNTF plays a role in promoting glial scar formation following spinal cord injury. The antibody closure model can be used to inhibit CNTF expression following spinal cord injury, thereby furthering the understanding of the role of CNTF in spinal cord injury repair. In the present experiment, spinal catheters were placed in the vertebral canal of spinal cord transected rats, and CNTF antibodies were injected following fixation of the paraspinal muscle catheter. At 24 hours after a single CNTF antibody injection, CNTF expression decreased in the thoracic and lumbar spinal cord and recovered to normal levels by 48 72 hours. CNTF antibody treatment can effectively block endogenous CNTF expression in the thoracic and lumbar spinal cord during an interval of less than 24 hours in transected rats.