Establishment and Evaluation of a Rat Model of Spinal Cord Injury with the Pathopattern of Qi-Deficiency and Blood-Stasis in Traditional Chinese Medicine

Objective To establish a rat model of Spinal Cord Injury(SCI)with the pathopattern of Qi-deficiency and Blood-stasis(QDBS)in Traditional Chinese Medicine(TCM),and then assess its feasibility.Methods Swimming exhaustion method and Rubrospinal Tract(RST)transection were combined to establish arat model of SCI with pathopattern of QDBS in TCM.Macroscopic representation,including the body weight,food intake and tongue scores,was recorded.Behavioristics was scored with spontaneous vertical exploration test.Hemorrheology was analyzed using hemorheological analyzer and morphology of spinal cord was observed.The feasibility of the model was confirmed on the basis of the reversion caused by administration of Bu Yang Huan Wu Decoction(BYHWD).Results The findings in the QDBS group were consistent with the symptoms of QDBS syndrome,including reduced body weight,food intake,and forelimb utilization rate and increased tongue scores.However,the corresponding findings in the BYHWD group were superior to those in the QDBS group after35d(P<0.05).In comparison with the control group,the QDBS group showed higher whole blood viscosity and hematocrit values(P<0.05)and a lower red blood cell(RBC)deformability index(P<0.05),while the corresponding findings in the BYHWD group were close to those in the control group.An eminence or induration appeared in the injured spinal cord,which was suspected to be vacuoles or a scar.Hematoxylin-eosin staining showed that the R/T ratio in the BYHWD group was higher than that in the QDBS group(P<0.05).Conclusion Swimming exhaustion method combined with RST transection operation can successfully establish a rat model of SCI with pathopattern of QDBS.

Neural Mechanism Underlying Task-Specific Enhancement of Motor Learning by Concurrent Transcranial Direct Current Stimulation

The optimal protocol for neuromodulation by transcranial direct current stimulation(tDCS)remains unclear.Using the rotarod paradigm,we found that mouse motor learning was enhanced by anodal tDCS(3.2 mA/cm^(2))during but not before or after the performance of a task.Dual-task experiments showed that motor learning enhancement was specific to the task accompanied by anodal tDCS.Studies using a mouse model of stroke induced by middle cerebral artery occlusion showed that concurrent anodal tDCS restored motor learning capability in a task-specific manner.Transcranial in vivo Ca^(2+)imaging further showed that anodal tDCS elevated and cathodal tDCS suppressed neuronal activity in the primary motor cortex(M1).Anodal tDCS specifically promoted the activity of task-related M1 neurons during task performance,suggesting that elevated Hebbian synaptic potentiation in task-activated circuits accounts for the motor learning enhancement.Thus,application of tDCS concurrent with the targeted behavioral dysfunction could be an effective approach to treating brain disorders.