大鼠脊髓损伤后前肢功能训练可塑性变化的可能发生机制

目的：探讨大鼠脊髓损伤(SCI)后前肢功能训练引起可塑性变化的可能机制。方法：在立体定位仪的引导下,致伤大鼠双侧红核和皮质脊髓背侧束(dCST)后,对大鼠行前肢功能训练6周。生物素化葡聚糖胺示踪皮质脊髓腹侧束(vCST)的出芽情况,免疫组化检测CST投射神经元(CSNs)生长相关蛋白_(43)(GAP_(43))和神经营养素共同受体P75(P75~(NTR))的表达,荧光金逆行示踪CSNs存活情况。结果：大鼠SCI后,前肢功能训练可诱导vCST出芽增加,上调CSNs GAP43和P75~(NTR)的表达,减少CSNs死亡。结论：大鼠CSI后,前肢功能训练增强可塑性变化的可能机制包括上调CSNs GAP43和P75~(NTR)的表达,减少CSNs死亡的发生。

Possible mechanisms of enhanced plasticity by forelimb training after spinal cord injury in rats

Objective:To explore the possible mechanisms of enhanced plasticity by forelimb training after spinal cord injury(SCI)in rats.Methods:Stereotaxieally,red nuclei and cervical dorsal corticospinal tract(dCST)were in- jured.Then rats accepted forelimb training for successive 6 weeks.Biotin Dextran Amine was employed to trace the sprouting of ventral eorticospinal traet(vCST).The expression of growth-associated protein(GAP_(43))and P75~(NTR) in eorticospinal neurons(CSNs)was evaluated by immunocytochemistry,and the survival of CNAs was vis- ualized by Fluord-Gold.Results:Forelimb training could enhance the sprouting of uninjured vCST,and could up regulate the expression of GAP_(43) and P75~(NTR) in CSNs.Also,it could reduce the death of CSNs.Conclusions:The possible mechanisms of enhanced plasticity by forelimb training after SCI in rats might include.(i)to up-regulate the expression of certain genes needed to enhance the CSNs potential for plasticity,such as GAP_(43) and P75~(NTR);(ii) to rescue CSNs from axotomy-induced death.