脊髓损伤后神经网络重建是未解决的关键科学问题，原因是大脑皮质脊髓束（CST）轴突与脊髓靶神经元形成突触的内在动力不足。联合应用促突触形成的粘附分子与神经干细胞(NSC)源性神经元移植是解决问题的关键策略。我们已证实：1.过表达聚集蛋白（agrin）粘附分子的神经元突起能够与过表达酪氨酸激酶（MuSK）的神经元形成突触样结构，但机制不清；2.移植NSC源性神经网络到脊髓损伤处，可部分改善脊髓功能。本研究将在全横断脊髓损伤处移植NSC源性神经网络组织，促进过表达agrin的再生CST(agrin-CST)轴突靶向与神经网络组织中过表达MuSK的神经元形成突触连接，促使NSC源性神经网络组织更好地传递脑源性神经信息，改善瘫痪肢体运动功能；同时探讨agrin-CST轴突靶向支配移植的NSC源性神经网络组织MuSK阳性神经元的机制，为应用agrin联合干细胞移植修复脊髓损伤的临床前研究提供理论依据。

The reconstruction of neural network after spinal cord injury is a key unsolved scientific problem, because of the lack of intrinsic power of the synapse between the axon of corticalspinal tract (CST) and the target neurons of spinal cord. The key strategy to solve this problem is to combine synaptic promoting adhesion molecules and NSC derived neurons. We have confirmed that: 1. The neurites of overexpressed adhesion molecule agrin can form synaptic structure with overexpressed MuSK neurons, but the mechanism is unclear; 2. Transplanting NSC-derived neural network to the spinal cord injury can partially improve the spinal cord function. In this study, NSC-derived neural network was transplanted into the transected spinal cord, so as to promote the axon of CST of overexpressed agrin to form synapse connection with the neurons overexpressed MuSK in the neural network, to transmit brain-derived neural information to NSC-derived neural network and improve the motor function of paralyzed limbs. At the same time, The mechanism of agrin navigating regenerative corticalspinal tract axons to the transplanted NSC-derived MuSK positive neurons and target innervation were discussed, which can provide theoretical basis for the preclinical study of repairing spinal cord injury with agrin combined with stem cell transplantation.