神经病理性疼痛是脊髓损伤（SCI）后的常见并发症。研究发现，SCI可导致脊髓内γ氨基丁酸（GABA）和谷氨酸（Glu）的比例失衡，促进神经病理性疼痛发生，其机制可能与胶质源性神经营养因子（GDNF）/谷氨酸转运体（GLTs）减少和GABA/Glu-Gln循环障碍有关。我们前期研究发现，运动可增加脊髓内GDNF、GLTs和GABA的合成，减轻SCI后的神经病理性疼痛，但具体调控机制不清。因此我们假设：运动训练可通过GDNF/GLTs调节GABA/Glu-Gln循环，改善SCI后神经病理性疼痛。为验证该假说，我们将采用SCI大鼠疼痛模型和体外细胞培养，探讨GDNF/GLTs在运动训练改善SCI后神经病理性疼痛中的作用，以及GDNF/GLTs对GABA/Glu-Gln循环的调控机制。本研究将有助于明确运动训练改善SCI后神经病理性疼痛的作用机制，为SCI后神经病理性疼痛的康复治疗提供理论依据。

Neuropathic pain is a common complication after spinal cord injury (SCI). Previous studies have shown that the imbalance of gamma aminobutyric acid (GABA)/glutamate (Glu) ratio in the spinal cord may promote the occurrence of neuropathic pain after SCI, and the mechanism may be related to the reduction of glial-derived neurotrophic factor (GDNF)/glutamate transporters (GLTs) and the disturbance of GABA/Glu-Gln cycle. Our previous study found that exercise training could increase the synthesis of GDNF, GLTs and GABA in the spinal cord and alleviate neuropathic pain after SCI, but the specific regulatory mechanism is unclear. Therefore, we hypothesized that exercise training could regulate GABA/Glu-Gln cycle through GDNF/GLTs and reduce neuropathic pain after SCI. To test this hypothesis, we will use SCI rat pain model and in vitro cell culture to explore the role of GDNF/GLTs in improving neuropathic pain after SCI by exercise training, and the regulatory mechanism of GDNF/GLTs on GABA/Glu-Gln cycle. This study will help to clarify the mechanism of exercise training in alleviating neuropathic pain after SCI, and provide a theoretical basis for the rehabilitation treatment of neuropathic pain after SCI.