Anastasia Agustín, de Erausquin Gabriel A, Wojnacki José, Mascó Daniel H
Centro de Biología Celular y Molecular. F.C.E.F.y N. Universidad Nacional de Córdoba, Córdoba, Argentina.
J Neurochem. 2007 Nov;103(4):1542-52. doi: 10.1111/j.1471-4159.2007.04856.x. Epub 2007 Sep 13.
Electroconvulsive shock (ECS) improves motor function in Parkinson's disease. In rats, ECS stimulates the expression of various factors some of which have been proposed to exert neuroprotective actions. We have investigated the effects of ECS on 6-hydroxydopamine (6-OHDA)-injected rats. Three weeks after a unilateral administration of 6-OHDA, 85-95% nigral dopaminergic neurons are lost. Chronic ECS prevented this cell loss, protect the nigrostriatal pathway (assessed by FloroGold retrograde labeling) and reduce motor impairment in 6-OHDA-treated animals. Injection of 6-OHDA caused loss of expression of glial cell-line derived neurotrophic factor (GDNF) in the substantia nigra. Chronic ECS completely prevented this loss of GDNF expression in 6-OHDA-treated animals. We also found that protected dopaminergic neurons co-express GDNF receptor proteins. These results strongly suggest that endogenous changes in GDNF expression may participate in the neuroprotective mechanism of ECS against 6-OHDA induced toxicity.
电惊厥休克（ECS）可改善帕金森病的运动功能。在大鼠中，ECS刺激多种因子的表达，其中一些因子已被认为具有神经保护作用。我们研究了ECS对注射6-羟基多巴胺（6-OHDA）大鼠的影响。单侧注射6-OHDA三周后，85-95%的黑质多巴胺能神经元丧失。慢性ECS可防止这种细胞丧失，保护黑质纹状体通路（通过荧光金逆行标记评估），并减少6-OHDA处理动物的运动障碍。注射6-OHDA导致黑质中胶质细胞源性神经营养因子（GDNF）表达丧失。慢性ECS完全防止了6-OHDA处理动物中GDNF表达的这种丧失。我们还发现受保护的多巴胺能神经元共表达GDNF受体蛋白。这些结果强烈表明，GDNF表达的内源性变化可能参与ECS对抗6-OHDA诱导毒性的神经保护机制。
