Responses to reversible anoxia of intracellular free and bound Ca2+ in rat cortical slices

Semenov, D. G.; Самойлов, М. О.; Zielonka, Piotr; Łazarewicz, Jerzy W.

doi:10.1016/s0300-9572(00)00136-2

Cited by 19 publications

(9 citation statements)

References 44 publications

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“…Due to their mild extent and highly probable signalling role, calcium transients evoked by PA should be attributed to physiological, regulatory phenomena. Changes in Ca i and Ca b induced by TA have been characterised and discussed in our previous study, demonstrating their sensitivity to NMDA receptor antagonists [20]. Calcium transients evoked by prolonged 10-min TA, which are much more pronounced, certainly represent pathological, potentially harmful mechanisms, and their prevention by PA reflects induced anoxic tolerance.…”

Section: Discussionmentioning

confidence: 87%

“…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: 88%

“…A CTC-Ca 2+ signal probably originates from the membranes of the endoplas-mic reticulum and mitochondria, as well as from a great number of calcium-binding proteins [26]. The utility and methodological matters connected with the analysis of Ca i and Ca b using fura-2 and CTC in brain slices has been extensively discussed elsewhere [20].…”

Section: Discussionmentioning

confidence: 99%

“…The procedures have previously been described in detail [20]. To avoid photobleaching of the calcium-sensitive dyes and photochemical injury of the tissue, measurements were performed every 5 min, each for a maximum of 5 s.…”

Section: Measurements Of Intracellular Free and Bound Calciummentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Section: Measurements Of Intracellular Free and Bound Calciummentioning

confidence: 99%

See 2 more Smart Citations

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

2002

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“…The methodical procedure initiating tolerance of the brain to hypoxia received the name "hypoxic preconditioning". Our previous studies showed that long-term (10 min) anoxia of slices of the olfactory cortex from rats induces sustained hyperactivation of NMDA receptors and pathological calcium overload of neurons [13]. Preconditioning of slices with short-term anoxia performed 90 min before long-term anoxia mobilizes the immediate mechanisms of tolerance (including NMDA receptor-mediated mechanisms) and prevents pathological changes induced by long-term anoxia [3,14].…”

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confidence: 99%

Effect of in vivo hypoxic preconditioning on changes in intracellular calcium content induced by long-term anoxia in rat brain slices

2004

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We studied changes in intracellular calcium content induced by 10-min anoxia in olfactory cortex slices from rats exposed to single or 3-fold moderate hypobaric hypoxia ("ascend" at 5000 m). Repeated preconditioning with moderate hypobaric hypoxia produced a neuroprotective effect. This treatment abolished pathological calcium overload in brain slices induced in vitro by 10-min test anoxia.Much attention is paid to the phenomenon of brain resistance to ischemia/hypoxia [2,3,9,15]. Moderate hypoxia increases the resistance of brain neurons to further exposure to severe hypoxia or ischemia. The methodical procedure initiating tolerance of the brain to hypoxia received the name "hypoxic preconditioning". Our previous studies showed that long-term (10 min) anoxia of slices of the olfactory cortex from rats induces sustained hyperactivation of NMDA receptors and pathological calcium overload of neurons [13]. Preconditioning of slices with short-term anoxia performed 90 min before long-term anoxia mobilizes the immediate mechanisms of tolerance (including NMDA receptor-mediated mechanisms) and prevents pathological changes induced by long-term anoxia [3,14]. In vivo moderate hypoxia is an adequate model of preconditioning. Successful preventive strategy requires estimating the "dose" of in vivo hypoxic preconditioning, i.e., depth and duration of hypoxia and period of the development and persistence of a neuroprotective effect. These studies were previously performed in vitro [2][3][4]15]. Two-step experiment is suitable for the search of optimal regimen of hypoxic preconditioning and study the induced intracellular neuroprotective mechanisms.The animal is subjected to moderate hypobaric hypoxia, and then cultured brain slices are in vitro exposed to long-term anoxia [1].Here we studied whether preconditioning with moderate hypobaric hypoxia can increase the resistance of brain neurons to calcium overload induced by test anoxia in brain slices from experimental animals. We also compared the neuroprotective effects of repeated and single hypobaric preconditioning. We recorded changes in intracellular calcium content induced by test anoxia in brain slices from rats exposed to different regimens of preconditioning with moderate hypobaric hypoxia. MATERIALS AND METHODSExperiments were performed on male Wistar-Kyoto rats weighing 190-210 g. The animals were divided into 2 groups. Group 1 rats were exposed to single preconditioning with hypobaric hypoxia. Pressure in a flow altitude chamber was maintained at a level of 380 mm Hg for 2 h (corresponds to an altitude of 5000 m above see level). In group 2 rats this procedure was repeated 3 times with 24-h intervals. Non-preconditioned animals served as the control.The 2nd stage of the study was performed in vitro on the next day after preconditioning. The rats were decapitated and tangential slices of the olfactory cor-

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Neuroprotective Interactions Between Delta-Opioid Receptors and Glutamatergic Signaling Mediate Hypoxia-Tolerance in Brain

Pamenter

2015

Neural Functions of the Delta-Opioid Receptor

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Responses to reversible anoxia of intracellular free and bound Ca2+ in rat cortical slices

Cited by 19 publications

References 44 publications

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

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

Effect of in vivo hypoxic preconditioning on changes in intracellular calcium content induced by long-term anoxia in rat brain slices

Neuroprotective Interactions Between Delta-Opioid Receptors and Glutamatergic Signaling Mediate Hypoxia-Tolerance in Brain

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