Dalia A, Neff N H, Hadjiconstantinou M
Department of Pharmacology, Ohio State University College of Medicine, Columbus 43210.
J Neurosci. 1993 Jul;13(7):3104-11. doi: 10.1523/JNEUROSCI.13-07-03104.1993.
Rat embryonic mesencephalic cultures were employed to evaluate the consequences of adding GM1 ganglioside to cultures lesioned with the selective neurotoxin 1-methyl-4-phenylpyridinium (MPP+). MPP+ reduced dopamine and DOPAC content, dopamine uptake, aromatic L-amino acid decarboxylase activity, and the number of tyrosine hydroxylase-immunopositive neurons. The immunopositive neurons that remained were aberrant. All of these parameters were partially restored by adding GM1 ganglioside to the cultures. The response to GM1 was not altered by prior treatment of the cultures with cytosine beta-D-arabinofuranoside to reduce the number of glial cells. Dopamine uptake activity restored by GM1 was lost if GM1 was removed from the culture.
采用大鼠胚胎中脑培养物来评估向用选择性神经毒素1-甲基-4-苯基吡啶鎓(MPP+)损伤的培养物中添加GM1神经节苷脂的后果。MPP+降低了多巴胺和DOPAC含量、多巴胺摄取、芳香族L-氨基酸脱羧酶活性以及酪氨酸羟化酶免疫阳性神经元的数量。残留的免疫阳性神经元是异常的。通过向培养物中添加GM1神经节苷脂,所有这些参数都得到了部分恢复。用β-D-阿拉伯呋喃糖胞苷预先处理培养物以减少神经胶质细胞数量,对GM1的反应并未改变。如果从培养物中去除GM1,GM1恢复的多巴胺摄取活性就会丧失。