海人酸、使君子酸致Huntington病鼠纹状体NOS阳性细胞的变化

THE CHANGES OF NOS POSITIVE CELLS IN THE RAT STRIATUM AFTER INJECTION OF KA OR QA

为了研究海人酸和使君子酸对大鼠纹状体 NOS阳性细胞的影响 ,用神经毒海人酸、使君子酸破坏大鼠左侧尾壳核 ,将夜间活动超过 6 0 0次、主动回避试验阳性率在 35 %以下的大鼠作为成功的 Huntington舞蹈病模型。注射后 2个月 ,将动物脑切片进行 Nissl、NADPH-d组化和 GF AP免疫组化反应。结果表明 ,海人酸和使君子酸均可使纹状体 n NOS阳性神经元丢失、出现i NOS阳性胶质细胞和侧脑室扩大 ,两者无显著差异。在损伤中心区 n NOS阳性神经元减少甚至消失 ,但这种变化自中心向周围呈渐变趋势 ;i NOS阳性胶质细胞呈两种不同形态 :一类胞体略大而突起粗短 ,一类胞体小而突起相对较长。对侧纹状体及伤侧纹状体非损毁部均未见 NOS阳性胶质细胞 ;NADPH-d组化和 GFAP免疫组化双重反应表明一些 i NOS胶质细胞为 GFAP阳性胶质细胞。本研究提示 ,海人酸和使君子酸均可使纹状体 n NOS神经元减少消失 ,损毁区出现的 NOS阳性胶质细胞为诱导型神经胶质细胞 (i NOS)。海人酸和使君子酸所引起的

To study the changes of NOS positive cells in Kainic acid (KA) and Quisqualic acid(QA) injured striatum of rats, Huntington's disease(HD) animal models were established by two injections of Kainic acid or Quisqualic acid into the left caudate-putamen(CP) of rats. The animals whose night locomotor activity times were over 600 and active avoidance test percentage under 35% were considered successful animal models. Two months later animals were sacrificed for morphological examinations. Nissl, NADPH-d histochemistry and GFAP immunohistochemistry staining were employed. Both neurotoxins caused decrease of NOS positive neurons and appearance of iNOS glial cells with enlargement of lateral ventricle. NOS positive neurons almost disappeared at the lesion centre, but the impairment was transitional. The iNOS positive glial cells in the lesioned area were divided into two different types: one with larger cell body and stubby processes, the other with smaller cell body and longer processes. No NOS positive glial cells were present in the uninjured area of lesioned striatum and the contralateral normal striatum. NADPH-d histochemistry and GFAP immunohistochemistry double staining showed some iNOS glial cells are GFAP positive glial cells. so the NOS positive gilal cells are inducible NOS cells(iNOS). There was no obvious behavioral and morphological difference between KA and QA established HD rat model.