Ramírez-Jarquín Uri Nimrod, Tapia Ricardo
División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, 04510-México, D.F., Mexico.
División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, 04510-México, D.F., Mexico.
Neuroscience. 2016 Sep 7;331:78-90. doi: 10.1016/j.neuroscience.2016.06.021. Epub 2016 Jun 16.
Motor neuron (MN) diseases are characterized by progressive cell degeneration, and excitotoxicity has been postulated as a causal factor. Using two experimental procedures for inducing excitotoxic spinal MN degeneration in vivo, by acute and chronic overactivation of α-amino-3-hydroxy-5-methyl-4-isoxazoleacetic acid (AMPA) receptors, we characterized the time course of the neuropathological changes. Electron transmission microscopy showed that acute AMPA perfusion by microdialysis caused MN swelling 1.5h after surgery and lysis with membrane rupture as early as 3h; no cleaved caspase 3 was detected by immunochemistry. Chronic AMPA infusion by osmotic minipumps induced a slow degeneration process along 5days, characterized by progressive changes: endoplasmic reticulum swelling, vacuolization of cytoplasm, vacuole fusion and cell membrane rupture. Quantification of these ultrastructural alterations showed that the increase of vacuolated area was at the expense of the nuclear area. Caspase 3 cleavage was observed since the first day of AMPA infusion. We conclude that acute AMPA-induced excitotoxicity induces MN loss by necrosis, while the progress of degeneration induced by chronic infusion is slow, starting with an early apoptotic process followed by necrosis. In both the acute and chronic procedures a correlation could be established between the loss of MN by necrosis, but not by caspase 3-linked apoptosis, and severe motor deficits and hindlimb paralysis. Our findings are relevant for understanding the mechanisms of neuron death in degenerative diseases and thus for the design of pharmacological therapeutic strategies.
运动神经元(MN)疾病的特征是进行性细胞变性,兴奋性毒性被认为是一个致病因素。我们采用两种在体内诱导兴奋性毒性脊髓MN变性的实验方法,即通过急性和慢性过度激活α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)受体,来描述神经病理学变化的时间进程。电子透射显微镜显示,通过微透析急性灌注AMPA在手术后1.5小时导致MN肿胀,最早在3小时出现膜破裂溶解;免疫化学检测未发现裂解的半胱天冬酶3。通过渗透微型泵慢性输注AMPA诱导了一个持续5天的缓慢变性过程,其特征为渐进性变化:内质网肿胀、细胞质空泡化、空泡融合和细胞膜破裂。对这些超微结构改变的量化显示,空泡化区域的增加是以核区域为代价的。自AMPA输注第一天起就观察到半胱天冬酶3的裂解。我们得出结论,急性AMPA诱导的兴奋性毒性通过坏死诱导MN丢失,而慢性输注诱导的变性进展缓慢,始于早期凋亡过程,随后是坏死。在急性和慢性过程中,坏死导致的MN丢失(而非半胱天冬酶3相关凋亡导致的MN丢失)与严重运动功能障碍和后肢麻痹之间均存在相关性。我们的研究结果对于理解退行性疾病中神经元死亡的机制以及药物治疗策略的设计具有重要意义。