Using the pyroantimonate method for precipitating calcium to electron-dense calcium pyroantimonate, the ultrastructural distribution of calcium was evaluated following single and repeated ischemic insults, produced by bilateral occlusions of common carotid artery in gerbils. Our observations revealed an excessive accumulation of calcium deposits in the mitochondria of pyramidal cell dendrites preceding their destruction. Following the disappearance of pyramidal cells, which becomes evident approximately 3 days after ischemic insults, a striking accumulation of electron-dense calcium deposits was observed in the dendrites of the interneurons, whereas mitochondria of these dendrites were free of calcium. Occasionally the reverse was true and calcium deposits were conspicuous in the center of mitochondria with well preserved cristae, whereas there was no calcium in the cytosol of the dendrites. The pattern of calcium distribution in the dendrites appears similar to that observed following convulsive seizures and indicates a possibility of neuroexcitatory mechanisms playing an important role in accumulation of calcium in injured by ischemia neurons. Otherwise, the intraneuronal presence of calcium itself does not seem to be invariably associated with a neuronal death.

National Institute of Health (NIH)
National Institute of Neurological Disorders and Stroke (NINDS)
Intramural Research (Z01)
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