GM1神经节苷脂诱导MPTP后黑质纹状体多巴胺能神经元的恢复：一项免疫组织化学研究

GM1 ganglioside-induced recovery of nigrostriatal dopaminergic neurons after MPTP: an immunohistochemical study.

作者信息

Hadjiconstantinou M, Mariani A P, Neff N H

机构信息

Department of Pharmacology, Ohio State University College of Medicine, Columbus 43210.

出版信息

Brain Res. 1989 Apr 10;484(1-2):297-303. doi: 10.1016/0006-8993(89)90373-9.

DOI:10.1016/0006-8993(89)90373-9

PMID:2565752

Abstract

The administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to mice results in the loss of dopamine (DA) and 3,4-dihydroxyphenylacetic acid (DOPAC) from the mouse striatum and a loss of cells containing tyrosine hydroxylase (TH)-immunoreactivity from the substantia nigra. The cells that remained in the nigra after MPTP treatment were smaller in diameter than normal cells. Treatment with GM1 ganglioside beginning 24 h after establishing the MPTP lesion resulted in partial restoration of DA and DOPAC content in the striatum and an increase in the diameter of the TH-immunoreactive nigra cells. It appears, therefore, that treatment of MPTP-intoxicated mice with GM1 ganglioside results in the partial restoration of both the biochemistry and morphology of dopaminergic neurons.

摘要

给小鼠注射1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）会导致小鼠纹状体中多巴胺（DA）和3,4-二羟基苯乙酸（DOPAC）减少，以及黑质中含酪氨酸羟化酶（TH）免疫反应性的细胞丧失。MPTP处理后黑质中残留的细胞直径比正常细胞小。在MPTP损伤形成后24小时开始用GM1神经节苷脂治疗，可使纹状体中DA和DOPAC含量部分恢复，并使TH免疫反应性黑质细胞的直径增加。因此，用GM1神经节苷脂治疗MPTP中毒的小鼠似乎可使多巴胺能神经元的生物化学和形态学部分恢复。