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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 Huntington病模型鼠形态学及行为变化均无明显差异
In order to study the effects of kainic acid and acidogenic acid on NOS positive cells in rat striatum, neurotoxin kainate was used to destroy the left caudate putamen nucleus in rats. Avoiding the test positive rate below 35% of rats as a successful Huntington chorea model. Two months after injection, the animal brain sections were subjected to Nissl, NADPH-d histochemistry and GF AP immunohistochemistry. The results showed that both kainic acid and gentamicin could cause the loss of nNOS positive neurons in the striatum. There was no significant difference in iNOS positive glial cells and lateral ventricle. NOS-positive neurons decreased or even disappeared in the injured area, but the change gradually changed from the center to the periphery. INOS-positive glial cells showed two different morphologies: Small and protruding relatively long. NOS positive glial cells were not found in the contralateral striatum and non-lesioned corpus striatum. NADPH-d staining and GFAP immunohistochemistry showed that some iNOS glial cells were GFAP-positive glia. This study suggests that kainic acid and gentamicin can reduce the number of nNOS neurons in the striatum disappeared, and the NOS positive glial cells in the damaged area are inducible glial cells (iNOS). There was no significant difference in morphological and behavioral changes in Huntington’s disease model rats induced by kainic acid and acid