Global brain ischemia and reperfusion: Golgi apparatus ultrastructure in neurons selectively vulnerable to death

Abstract

The neocortex and the hippocampus were examined for lipid peroxidation products and ultrastructural alterations by fluorescence and electron microscopy, respectively, in rats subjected to 10 min of cardiac arrest or 10 min cardiac arrest and either 90 or 360 min reperfusion. Lipid peroxidation products were observed after 90 min reperfusion in the perikarya and proximal dendrites of neocortical pyramidal neurons and in the hippocampal hilar cells and CA1, region; the fluorescence was most intense at the base of the apical dendrite, the region of the Golgi apparatus. After 90 min of reperfusion, the CA1, showed considerable stretches of rough endoplasmic reticulum devoid of ribosomes and the Golgi cisternae were shorter and widely dilated. The neocortex showed similar endoplasmic reticulum changes, but no significant alterations to the Golgi were noted. In addition there were areas where strings of ribosomes appear to be detaching from the endoplasmic reticulum. After 360 min reperfusion in both the neocortex and the hippocampus, the damage appeared more severe. The Golgi was fragmented into vacuoles, membranous whorls had appeared, and dense aggregates of smooth vesicles were seen coalescing with each other and the vacuoles. These observations suggest that early Golgi involvement is a more important marker of lethal injury than ribosome release from the endoplasmic reticulum. The areas of disturbed Golgi ultrastructure correspond to those areas that show evidence of lipid peroxidation and imply that lipid peroxidation may be causally related to the disturbance in Golgi ultrastructure.

Inhibition of Sevoflurane Postconditioning Against Cerebral Ischemia Reperfusion-Induced Oxidative Injury in Rats

“…During the 48–72 h delay period, the neurons destined to die look normal under the light microscope. At the ultrastructural level, however, disaggregation of polyribosomes, abnormalities of the Golgi apparatus, deposition of dark substances, and modification of postsynaptic densities have been reported [ 60 , 61 , 62 , 63 , 64 ].…”

Insulin like growth factor-1 (IGF-1) decreases ischemia-reperfusion induced apoptosis and necrosis in diabetic rats

“…Pyramidal neurons in the CA1 and CA3 regions of the hippocampus and those in layers III and V of the cerebral cortex are also selectively vulnerable to death after injury by ischemia and reperfusion [23]. Ultrastructural evidence have demonstrated that most of the damage associated with reperfusion in vulnerable neurons involves disaggregation of polyribosomes, peroxidative damage to unsaturated fatty acids in the plasma membrane, and distinct alterations in the structure of the Golgi apparatus that is responsible for membrane assembly [24]. In addition, as a result of reperfusion, inhibition of protein synthesis, involving alteration of the translation initiation factors, specifically serine phosphorylation of the alpha subunit of eukaryotic initiation factor-2 (eIF-2 alpha), result in death of the selectively vulnerable neurons [23].…”

Changes in cerebellar purkinje cells during postresuscitation period: Morphometric and ultrastructural analysis

“…After 7 days these changes involved only EPR whose tubules were markedly widened, which can be associated with inhibition of protein synthesis in the cell. EPR dysfunction after shortterm ischemia was reported by other authors [12,13]. The ultrastructure of PC improved by day 14, but 1 month after resuscitation degenerative processes were enhanced again: numerous lysosomes and swollen mitochondria appeared.…”