Neuronal susceptibility to damage: comparison of the retinas of young, old and old/caloric restricted rats before and after transient ischemia
Neuronal susceptibility to damage: comparison of the retinas of young, old and old/caloric restricted rats before and after transient ischemia
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DOI：
10.1016/j.neurobiolaging.2003.07.005
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发表时间：
2004-04-01
影响因子：
4.2
通讯作者：
Neufeld, AH
中科院分区：
文献类型：
--
作者：
Kim, KY;Ju, WK;Neufeld, AH
与年轻大鼠相比，老年增加视网膜缺血/再灌注后视网膜神经节细胞和移位无长突细胞丢失的易感性和热量限制降低易感性。在缺血前老年动物的视网膜中，与年轻和老年/热量限制动物的视网膜相比，反应性神经胶质增生，包括Muller细胞、小胶质细胞和星形胶质细胞的活化增加。缺血后，老年动物视网膜中存在的反应性神经胶质增生不具有神经保护作用，并且与年轻或老年/热量限制的动物相比，老年动物中的反应性神经胶质增生甚至进一步增加。在视网膜从老/热量限制的动物，诱导热休克蛋白-70和脑源性神经营养因子增加更显着缺血/再灌注后的视网膜相比，从年轻和年老的动物。因此，与年轻动物的视网膜相比，老年动物的神经元在视网膜缺血/再灌注后可能更容易受到继发性胶质机制的细胞死亡。限制老年动物的热量摄入对缺血后视网膜损伤具有神经保护作用，这可能是通过抑制胶质细胞活性以及诱导型热休克蛋白-70和脑源性神经营养因子的神经保护作用实现的。(C)2003年爱思唯尔公司All rights reserved.
Compared to young rats, old age increases susceptibility and caloric restriction decreases susceptibility for the loss of retinal ganglion cells and displaced amacrine cells following retinal ischemia/reperfusion. In retinas of old animals before ischemia, reactive gliosis, including activation of Muller cells, microglia and astrocytes, is increased compared to retinas from young and old/caloric restricted animals. Post-ischemia, the existing reactive gliosis in retinas of old animals is not neuroprotective and the reactive gliosis is even further increased in old animals compared to young or old/caloric restricted animals. In retinas from old/caloric restricted animals, inducible heat shock protein-70 and brain-derived neurotrophic factor increased more markedly after ischemia/reperfusion compared to retinas from young and old animals. Thus, compared to retinas in young animals, neurons of old animals may be more susceptible to cell death by secondary glial mechanisms after retinal ischemia/reperfusion. Caloric restriction in old animals is neuroprotective against damage in the retina following ischemia, perhaps by suppressing glial activity and by the neuroprotective effects of inducible heat shock protein-70 and brain-derived neurotrophic factor. (C) 2003 Elsevier Inc. All rights reserved.