Barcia Carlos, Sánchez Bahillo Angel, Fernández-Villalba Emiliano, Bautista Víctor, Poza Y Poza Máximo, Fernández-Barreiro Andrés, Hirsch Etienne C, Herrero María-Trinidad
Experimental Neurology and Neurosurgery Group, Department of Human Anatomy and Psychobiology, School of Medicine, University of Murcia, Murcia, Spain.
Glia. 2004 May;46(4):402-9. doi: 10.1002/glia.20015.
Inflammatory changes have been found in Parkinson's disease, in humans intoxicated with the parkinsonian toxin MPTP, and in animal models of the disease. However, it is still not known whether inflammatory changes are responsible for active nerve cell death or if they have a protective role against neurodegeneration. In this study, we analyzed the glial reaction in the substantia nigra pars compacta (SNpc) and the striatum of monkeys rendered parkinsosian by chronic MPTP injections. At postmortem examination 1 year after the last MPTP injection, the density of astroglial cells and activated microglial cells in the SNpc, but not in the striatum, of MPTP-intoxicated animals was significantly higher than in the two control animals. These data suggest that neurodegeneration was still active despite the absence of the agent triggering cell death and that the glial reaction is associated with long-term neurodegeneration.
在帕金森病患者、被帕金森病毒素MPTP中毒的人类以及该疾病的动物模型中均发现了炎症变化。然而，目前仍不清楚炎症变化是导致神经细胞主动死亡的原因，还是对神经退行性变具有保护作用。在本研究中，我们分析了通过慢性注射MPTP诱导帕金森病的猴子黑质致密部（SNpc）和纹状体中的胶质反应。在最后一次注射MPTP后1年进行尸检时，MPTP中毒动物的SNpc中星形胶质细胞和活化小胶质细胞的密度显著高于两只对照动物，而纹状体中的密度则无显著差异。这些数据表明，尽管引发细胞死亡的因素已不存在，但神经退行性变仍在进行，且胶质反应与长期神经退行性变相关。
