中文摘要：

目的观察头孢曲松对甲基苯丙胺（METH）急性、亚急性处理时致神经损伤情况的影响，以及对伏隔核中谷氨酸转运体1（GLTl）与囊泡型谷氨酸转运体1（VGLUTl）的变化的影响。方法建立METH急性毒性模型，同时利用谷氨酸转运体调节剂头孢曲松调控谷氨酸转运体的表达，尼氏染色实验观测神经元中尼氏小体的变化，利用Westernblot实验检测其谷氨酸转运体蛋白表达的变化。结果METH急性给药组与盐水对照组相比，刻板行为明显增加（P〈0．01），尼氏小体明显减少；伏隔核中GLTl和VGLUTl的表达增加分别为53．7％和102％（P〈0．05）；头孢曲松预防给药组与METH组相比，大鼠刻板行为明显减少，伏隔核中GLTl的表达增加36％（P〈0．05）；VGLUTl的表达下调56％（P〈0．05）；METH亚急性处理后，与盐水对照组相比，伏隔核中GLTl的蛋白表达增加40．9％，VGLUTl蛋白表达增加52．9％；预防给予头孢曲松后，头孢曲松预防给药组与METH组相比，GLTl和VGLUTl蛋白表达差异没有显著性。结论METH处理导致神经损伤，引起伏隔核中谷氨酸转运体的表达变化；头孢曲松能激活谷氨酸转运体的表达，缓解METH引起的神经损伤。

英文摘要：

Aim To observe the role of ceftrixone on neuro-injury induced by methamphetamine （METH）a- cute/sub-acute treatment, and changes of glutamate transporter 1 （ GLT1 ） and vesicular glutamate transport-er 1 （ VGLUT1 ） in nucleus accumbens under different conditions. Methods Rats were administered （ ip ） with METH to establish acute and sub-acute toxicity model , and the glutamate transporter agonist ceftriaxone（Cef） was applied to regulate the expression of gluta- mate transporters. The neurotoxicity of METH was e- valuated by Nissl staining method and stereotyped be- havior. The expression of GLT1 protein and VGLUT1 protein was evaluated by Western blot. Results Com- pared to the saline group, stereotyped behaviors in METH acute-treated group significantly increased, and the density of nissl significantly reduced; the expres- sion of GLT1 protein and VGLUT1 protein in METH group was significantly up-ragulated by 53.7% and 102% （P 〈 0. 05 ） in nucleus accumbens ; compared to the METH group, pre-administration of ceftriaxone so- dium with METH decreased stereotyped behaviors, GLT1 protein expression was also siginificantly in-creased by 36%, and VGLUT1 protein expression was down-regulated by 56% （ P 〈 0. 05 ）. Compared to the saline group, the expression of GLT1 and VGLUT1 in nucleus accumbens of rats which sub-acuted treated by METH increased by 40. 9% and 52. 9%, and there was no significant diffierence in pre-administration of ceftriaxone sodium group and METH sub-acuted group. Conclusions Acute sub-acute administration of METH can cause nerve injury and dysregulation of glu- tamate transporters in striatum ; ceftriaxone which can regulate expression of glutamate transports can dilute nerve injury induced by METH.