【摘要】 用ＳＤ大鼠腹腔注射丙烯酰胺（ＡＣＲ）３周，观察其小脑功能损伤、组织形态学及某些生化损伤。结果：ＡＣＲ注射１周后出现共济失调、主动活动减少等症状，随注射时间延长上述症状进行性加重；３周后实验组小脑组织肌酸磷酸激酶（ＣＰＫ）和谷胱甘肽转移酶（ＧＳＴ）活性明显低于对照组（Ｐ＜０．０１）；组织学检查蒲肯野细胞退行性改变。研究证实，ＡＣＲ对小脑有选择性损伤作用，这种作用可能与小脑皮层蒲肯野细胞（ＰＣｓ）的高代谢水平及ＡＣＲ对小脑组织高亲和性有关。更多还原

【Abstract】 Acrylamide(ACR) is an potent neurotoxic agent, and ataxia is the most outstanding symptom of its intoxication in humans and experimental animals. In this trial, SD rats were administered ACR (30 mg/kg body wt) intraperitoneally daily, five times a week for 3 weeks. Progressive ataxia and decrease in motor activity were observed after the treatment. The symptoms became progressively worse with further treatment. After three consecutive weeks, treatment, the average creatine kinase (CPK) activity in cerebellar tissue was (8763.8±679.2) IU/g compared with (12491.7±900.8) IU/g in sham control group( P <0.01), and mean glutathone s transferase (GST) activity was (85.2±10.1) IU/g while (119.2±15.9) IU/g in sham control group in cerebellar tissue ( P <0.01). Histopathology demonstrated that cerebellar cortex of the sham control group exhibited a characteristic trilaminer structure with flask shaped Purkinje neurons connected with their apical dendrites. ACR treated cerebellum showed degenerating Purkinje neurons of variegated morphology, whose connection with their dendrites were rarely discernible. The trial testifievd the selective injury of ACR to cerebellum (especially to Purkinje neurons). This is perhaps related to the high affinity of ACR to cerebellum and high energic metabolic level in cerebellar cortex.更多还原