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用成年Ｗｉｓｔａｒ大鼠７０只，雌雄不拘，通过向腰髓内注射海人藻酸（５μｌ，０．００１ｍｏｌ／Ｌ）建立了脊髓内注射神经毒导致大鼠脊髓损伤的动物模型；一部分向脊髓内注射盐水做为对照．动物按注射后存活２ｈ、６ｈ、１２ｈ、２４ｈ、３ｄ、６ｄ和１４ｄ分组．Ｎｉｓｓｌ染色，电镜观察。注射后２４ｈ内，脊髓腹角神经元出现进行性细胞肿胀，尼氏作皱缩深染，形成许多微细的空泡，胞核浓缩。电镜下观察到内质网、线粒体和高尔基氏体的肿胀和胞质内的空泡和树突的膨胀．注射后３～６ｄ，神经细胞发生明显的退变，细胞质浓缩，尼氏体分解，早期病变的小空泡形成较大的空洞，核偏移。６ｄ后大部分细胞死亡，尚存的脊髓运动神经元明显肿胀，细胞核的边界不清，尼氏体完全消失，电镜下显示细胞器完全被破坏，胞质内的空洞进一步融合形成几个大空洞，细胞核继续浓缩。１４ｄ后注射部位的运动神经元几乎完全消失，胶质细胞明显增生。作为谷氨酸受体激动剂的海人藻酸导致脊髓运动神经元的急性溃变，可作为除撞击、压迫、缺血或横断所致脊髓损伤以外的又一种动物模型，其损伤的病理变化以神经元退变为主，而脊髓的完整性不受破坏，类似于脊髓灰质炎的病变，适用于神经细胞移植的研究。
Seventy adult Wistar rats were randomly divided into male and female rats. Animal models of spinal cord injury induced by intracerebroventricular injection of neurotoxicity were established by injecting kainic acid (5μl, 0.001mol / L) into the lumbar spinal cord. Saline was injected as a control. The animals survived 2h, 6h, 12h, 24h, 3d, 6d and 14d after injection. Nissl staining, electron microscopy. Within 24 hours after injection, neurons in the ventral horn of the spinal cord developed progressive cell swelling, and Nissl was crimped and dyed to form many fine vacuoles and nuclei were concentrated. Electron microscopy was observed in the endoplasmic reticulum, mitochondria and Golgi apparatus swelling and cytoplasmic vacuoles and dendrites expansion. At 3 ~ 6 days after injection, the neurons degenerated obviously, the cytoplasm was concentrated, the Nissl body decomposed, and the small vacuoles of early lesions formed larger cavities and nuclear deviations. After 6 days, most of the cells died, the remaining motor neurons in the spinal cord swell obviously, the boundary of the nucleus was unclear, the Nissl body disappeared completely, the organelles were completely destroyed by electron microscopy, and the vacuoles in the cytoplasm were further fused to form several large cavities. The nucleus continues to concentrate. Motor neurons at the injection site disappeared almost completely after 14d, and glial cells proliferated significantly. Kainic acid, a glutamate receptor agonist, causes acute degeneration of motor neurons in the spinal cord and serves as an animal model in addition to spinal cord injury due to impact, compression, ischemia, or transection, and the pathology of the lesion Changes in the main neuronal degeneration, while the integrity of the spinal cord is not damaged, similar to the lesions of poliomyelitis, suitable for nerve cell transplantation research.