论文部分内容阅读
目的探讨锰对小鼠基底核突触体谷氨酸(Glu)和γ-氨基丁酸(GABA)释放的影响。方法将24只健康清洁级昆明小鼠按体重随机分为4组,分别为对照(生理盐水)组和25、50、100μmol/kg氯化锰染毒组,每组6只,雌雄各半。采用腹腔注射方式进行染毒,每周染毒5次,连续染毒4周。测量小鼠基底核内的锰含量;并用15 mmol/L KCl诱发并测定基底核突触体Glu和GABA的释放量。结果与对照组比较,50、100μmol/kg氯化锰染毒组小鼠基底核锰含量均增加,差异有统计学意义(P<0.05)。且随着锰染毒剂量的升高,小鼠基底核锰含量呈上升趋势。与对照组比较,25、50μmol/kg氯化锰染毒组小鼠基底核突触体Glu的释放量均增加,100μmol/kg氯化锰染毒组小鼠基底核突触体Glu的释放量及50、100μmol/kg氯化锰染毒组小鼠基底核突触体GABA的释放量均下降,差异有统计学意义(P<0.05);且随着氯化锰染毒剂量的升高,小鼠基底核突触体Glu释放量呈先上升后下降的趋势,而GABA释放量呈下降的趋势。结论锰可在小鼠脑基底核内蓄积,并对基底核突触体谷氨酸和GABA释放产生影响,造成神经系统紊乱。
Objective To investigate the effect of manganese on the release of glutamic acid (Glu) and γ-aminobutyric acid (GABA) in basal ganglia in mice. Methods Twenty-four healthy Kunming mice were randomly divided into four groups according to body weight: control (saline) group and 25, 50 and 100μmol / kg manganese chloride exposure groups, 6 in each group with half male and half female. By intraperitoneal injection of exposure, 5 times a week, continuous exposure for 4 weeks. The amount of manganese in the basal nucleus of the mouse was measured. The amount of Glu and GABA released from basal ganglia was induced by 15 mmol / L KCl. Results Compared with the control group, the contents of manganese in basal ganglia in 50 and 100μmol / kg MnCl2-treated mice increased significantly, with statistical significance (P <0.05). And with the increase of manganese dose, the content of manganese in the basal nucleus of mice showed an upward trend. Compared with the control group, the amount of Glu released from the basal ganglia in 25 and 50μmol / kg MnCl2-treated mice increased, while that in the 100μmol / kg MnCl2-treated mice (P <0.05). The release of GABA in basal nucleus synaptosomes of mice exposed to 50 and 100μmol / kg MnCl2 decreased significantly (P <0.05). With the increase of the dose of manganese chloride, Glu release from basal ganglia in mice showed a tendency of first increasing and then decreasing, while the release of GABA tended to decrease. Conclusion Manganese accumulates in the basal ganglia in mice and affects the release of glutamate and GABA from basal synaptosomes, resulting in neurological disorders.