Changes of intracellular calcium homeostasis in brain cortical structures during anoxia in vivo and in vitro

Łazarewicz, Jerzy W.; Samoilov, Mikchail O.; Semenov, D. G.

doi:10.1016/0300-9572(87)90003-7

Cited by 10 publications

(4 citation statements)

References 19 publications

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“…Although the effects of hypoxia on calcium movements are well documented (23)(24)(25), our results, together with the lack of restoration of normal ATP production, indicates failure of the transporters to re-establish the normal Ca 2+ gradient.…”

Section: Discussioncontrasting

confidence: 69%

The Effect of Mild and Severe Hypoxia on Rat Cortical Synaptosomes

2005

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Brain ischemia results in neuronal injury and neurological disability. The present study examined the effect of mild (6% O2) and severe (2% O2) hypoxia on mitochondria of rat cortical synaptosomes. During mild and severe hypoxia, JO2 and ATP production significantly decreased and mitochondrial membranes depolarized. Synaptosomal calcium concentration increased slightly, albeit not significantly. After a 1 h re-oxygenation period, JO2, ATP production and mitochondrial membrane potential returned to control levels in synaptosomes incubated in 6% O2. In synaptosomes incubated in 2% O2, however, the ATP production was not restored after re-oxygenation and intrasynaptosomal Ca2+ significantly increased. The results indicate that both mild and severe hypoxia influence the physiology of synaptosomal mitochondria; the modifications are reversible after mild hypoxia and but partly irreversible after severe hypoxia.

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Section: Discussioncontrasting

confidence: 69%

The Effect of Mild and Severe Hypoxia on Rat Cortical Synaptosomes

2005

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“…Mobilisation of intracellular calcium ions and increased Ca i level in neurons during initial periods of anoxia/ischaemia have been described in several other papers [20,37,38]. The changes in Ca i and Ca b that develop during reoxygenation clearly result from a more complex mechanism involving activation of NMDA receptors, influx of extracellular Ca 2+ to neurons, increases in intracellular levels of free Ca 2+ ions and their intracellular binding giving rise to an increased Ca b .…”

Section: Discussionmentioning

confidence: 97%

Calcium Transients in the Model of Rapidly Induced Anoxic Tolerance in Rat Cortical Slices: Involvement of NMDA Receptors

2002

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In this study, we investigated the effects of NMDA receptor antagonists on calcium transients induced by a single 2-min preconditioning anoxia (PA) in rat olfactory cortical slices, and on the ability of PA to prevent pathological calcium overload induced by subsequent 10-min test anoxia (TA). Relative changes in the intracellular Ca²⁺ concentration (Ca_i) and in the level of Ca²⁺ bound to intracellular hydrophobic domains (Ca_b) were monitored using fura-2 and chlortetracycline, respectively. Our results confirmed that TA induces prominent long-lasting increases in Ca_i and Ca_b, reflecting cellular calcium overload. It was found that PA produces moderate increases in both Ca²⁺ pools and prevents Ca²⁺ overload induced by TA carried out 90 min later. Calcium transients and the protective effects of PA were significantly suppressed in slices treated with NMDA receptor antagonists during and 30 min after PA. These results indicate that moderate activation of the NMDA receptors participates in the mechanism of the PA-induced anoxic tolerance of cortical neurons.

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“…During and after hypoxia, the intracellular calcium concentration markedly increases due to inflow from interstitial spaces and release from intracellular stores, and the disruption of [Ca 2? ] i homeostasis plays a major role in ischemic neuronal injury [12,28]. Moreover, hypoxia is responsible for expression of pro-apoptotic proteins which depends on nuclear Ca 2?…”

Section: Discussionmentioning

confidence: 99%

The Effects of Hypoxia/Reoxygenation on the Physiological Behaviour of U373-Mg Astrocytes

et al. 2009

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Nerve cells are very susceptible to hypoxia responsive for mitochondrial dysfunctions involved in the subsequent oxidative stress, apoptosis and necrosis. In this paper, we examined the effect of 12 h incubation of U-373 MG astrocytes in hypoxic environment (73% N 2 : 2% O 2 : 5% CO 2 , v:v) by evaluating cell proliferation, modifications of NO and ATP production, intracellular Ca 2? concentration [Ca 2? ] i , membrane potential, desferoxaminechelatable free iron, esterified F2-isoprostanes levels and the production of phosphorylated ERK. The same parameters were evaluated also after a following re-oxygenation period of 24 h. Immediately after hypoxia the NO concentration increased significantly and returned to values similar to those of controls after the re-oxygenation period. At the same time, ATP levels remained similar to controls and the cell proliferation significantly decreased. This involved a significant increase of [Ca 2? ] i immediately after hypoxia and the value remained significantly elevated after the following re-oxygenation period. Moreover, after hypoxia, astrocytes were slightly although not significantly depolarized. Indeed iron and F2-isoprostanes levels increased significantly after hypoxia. Finally ERK proteins increased slowly and not significantly after hypoxia and the same trend was observed after the re-oxygenation period.On the whole, our results indicate that 2% O 2 hypoxia induces a moderate oxidative stress, well tolerated by U-373 MG cells, remaining the ATP production, mitochondrial membrane potential and activated ERK proteins, similar to the values of controls.

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Changes of intracellular calcium homeostasis in brain cortical structures during anoxia in vivo and in vitro

Cited by 10 publications

References 19 publications

The Effect of Mild and Severe Hypoxia on Rat Cortical Synaptosomes

The Effect of Mild and Severe Hypoxia on Rat Cortical Synaptosomes

Calcium Transients in the Model of Rapidly Induced Anoxic Tolerance in Rat Cortical Slices: Involvement of NMDA Receptors

The Effects of Hypoxia/Reoxygenation on the Physiological Behaviour of U373-Mg Astrocytes

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