Zurn A D, Baetge E E, Hammang J P, Tan S A, Aebischer P
Division de Recherche Chirurgicale, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
Neuroreport. 1994 Dec 30;6(1):113-8. doi: 10.1097/00001756-199412300-00030.
Glial cell line-derived neurotrophic factor (GDNF) has been postulated to be a specific dopaminergic neurotrophic factor since it selectively enhances the survival of dopaminergic neurones in vitro. We report here that GDNF can also act as a neurotrophic factor for motoneurones. GDNF released by GDNF-transfected BHK cells increases the activity of choline acetyltransferase (ChAT) in cultures from embryonic rat ventral mesencephalon containing cholinergic neurones from cranial motor nuclei and in cultured spinal motoneurones. Furthermore, local application of polymer-encapsulated BHK cells releasing GDNF to transected facial nerve in newborn rats diminishes the death of motoneurones normally occurring after axotomy in the neonatal period. The present results indicate that GDNF may have a therapeutic potential in human motoneurone diseases such as amyotrophic lateral sclerosis.
胶质细胞系源性神经营养因子（GDNF）自被发现能在体外选择性增强多巴胺能神经元的存活以来，一直被假定为一种特异性的多巴胺能神经营养因子。我们在此报告，GDNF也可作为运动神经元的神经营养因子。GDNF转染的BHK细胞释放的GDNF可增加来自胚胎大鼠腹侧中脑、含有来自颅运动核的胆碱能神经元的培养物以及培养的脊髓运动神经元中胆碱乙酰转移酶（ChAT）的活性。此外，将释放GDNF的聚合物包裹的BHK细胞局部应用于新生大鼠横断的面神经，可减少新生期轴突切断后通常发生的运动神经元死亡。目前的结果表明，GDNF在人类运动神经元疾病如肌萎缩侧索硬化症中可能具有治疗潜力。
