Experimental research on selective neuronal damage by methylmercury using microdissection method

采用显微解剖系统分离大鼠小脑颗粒神经元、浦肯野神经元和分子层神经元，实时荧光定量PCR检测抗氧化酶水平。结果表明，抗氧化酶（Mn-SOD、GPx1和TRxR1）的低表达导致了CGCs对MeHg的易感。接下来，神经行为分析显示，在发育期间暴露于低水平的甲基汞会导致大鼠运动协调能力的显著缺陷。突触素（synaptophysin，突触形成的标志蛋白）在小脑颗粒细胞中的表达显著降低。这些结果表明，在发育过程中暴露于低剂量甲基汞会引起小脑颗粒细胞突触稳态的改变，从而导致运动协调功能障碍。

We isolated granule, Purkinje and molecular layer's neurons in rat cerebellum by using microdissection system and performed real-time PCR analyses for anti-oxidative enzymes. The results suggest that low expression of anti-oxidative enzymes (Mn-SOD, GPx1 and TRxR1) causes CGCs vulnerability to MeHg toxicity.Next, neurobehavioral analyses revealed that exposure to a low level of MeHg during developmental caused a significant deficit in the motor coordination of rats. The expression of synaptophysin, a marker protein for synaptic formation, significantly decreased in cerebellar granule cells. These results showed that exposure to low-dose MeHg during development induces the dysfunction of motor coordination due to changes of synaptic homeostasis in cerebellar granule cells.