Hou J G, Lin L F, Mytilineou C
Department of Neurology, Mount Sinai School of Medicine, New York, New York 10029, USA.
J Neurochem. 1996 Jan;66(1):74-82. doi: 10.1046/j.1471-4159.1996.66010074.x.
The effect of glial cell line-derived neurotrophic factor (GDNF) on the growth of mesencephalic dopaminergic neurons and on their survival following exposure to the neurotoxin 1-methyl-4-phenylpyridinium (MPP+) was examined in vitro. In cultures developing under normal conditions, GDNF at 1 ng/ml optimally improved the survival and stimulated the growth of dopaminergic neurons without affecting glial growth. In cultures treated with MPP+, GDNF could not prevent toxicity to dopaminergic neurons. The uptake of [3H]dopamine and the number of tyrosine hydroxylase-positive neurons were similarly reduced by MPP+ in the presence or absence of GDNF. However, after removal of MPP+, GDNF protected dopaminergic neurons from the continuous cell death and stimulated the regrowth of dopaminergic fibers damaged by MPP+. We conclude that GDNF supports the growth of normally developing dopaminergic neurons and stimulates their survival and recovery after damage. These findings suggest that GDNF could be useful in the development of therapeutic approaches to Parkinson's disease, which is characterized by dopaminergic cell loss.
在体外研究了胶质细胞系源性神经营养因子(GDNF)对中脑多巴胺能神经元生长以及其在暴露于神经毒素1-甲基-4-苯基吡啶鎓(MPP +)后的存活情况的影响。在正常条件下发育的培养物中,1 ng/ml的GDNF能最佳地改善多巴胺能神经元的存活并刺激其生长,而不影响神经胶质细胞的生长。在用MPP +处理的培养物中,GDNF无法预防对多巴胺能神经元的毒性。无论有无GDNF,MPP +都会类似地降低[3H]多巴胺的摄取以及酪氨酸羟化酶阳性神经元的数量。然而,去除MPP +后,GDNF可保护多巴胺能神经元免于持续的细胞死亡,并刺激被MPP +损伤的多巴胺能纤维的再生。我们得出结论,GDNF支持正常发育的多巴胺能神经元的生长,并在损伤后刺激其存活和恢复。这些发现表明,GDNF可能有助于开发针对以多巴胺能细胞丢失为特征的帕金森病的治疗方法。