Microglial Reaction in MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) Induced Parkinson's Disease Mice Model

Anna Członkowska , Małgorzata Kohutnicka , Iwona Kurkowska-Jastrzębska , Andrzej Członkowski
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引用次数: 279

Abstract

We studied the microglial reaction in mice using the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced model for Parkinson's disease (PD). Microglial cells were identified by means of the Griffonia simplicifolia lectin (GSA-I-B4). Dopaminergic neurons were marked by tyrosine hydroxylase antibodies. Microglial activation was demonstrated by an increase in cellular number and changes of morphology (increased lectin staining, larger cell bodies and thicker processes) were seen in the substantia nigra from the 1st to the 14th day and in the striatum from the 1st to the 4th day after intoxication. Depletion of dopaminergic neurons was most pronounced 7 and 14 days following the treatment. The results suggest that microglial activation may be involved in the sequence of pathological changes that lead to dopaminergic neuronal damage after MPTP intoxication.

MPTP(1-甲基-4-苯基-1,2,3,6-四氢吡啶)诱导帕金森病小鼠模型的小胶质细胞反应
我们用1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导的帕金森病(PD)模型研究了小鼠的小胶质细胞反应。小胶质细胞用单纯格里菲尼亚凝集素(GSA-I-B4)鉴定。酪氨酸羟化酶抗体标记多巴胺能神经元。中毒后第1 - 14天,黑质和纹状体的小胶质细胞数量增加,形态改变(凝集素染色增加,细胞体变大,突起变厚),小胶质细胞活化。多巴胺能神经元的损耗在治疗后的第7天和第14天最为明显。结果提示,MPTP中毒后,小胶质细胞的激活可能参与了导致多巴胺能神经元损伤的一系列病理改变。
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