Hypoxic pretreatment protects against neuronal damage of the rat hippocampus induced by severe hypoxia

Gorgias, N.; Maidatsi, P.; Tsolaki, Magda; Alvanou, A.; Kiriazis, George; Kaidoglou, K.; Giala, M.

doi:10.1016/0006-8993(95)01548-5

Cited by 38 publications

(20 citation statements)

References 33 publications

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“…With hypoxic preconditioning, three separate studies using different experimental strategies all suggested that hypoxic tolerance, when present, was related to increased expression and activities of SODs (133,143,292). In contrast, ischemic preconditioning in rats induced sustained increased levels of SODs when induced by 5 min of four-vessel occlusion (86), but not when induced by 3-min MCAO (325).…”

Section: Sods (Mn-sod and Cu/zn-sod)mentioning

confidence: 99%

Molecular Physiology of Preconditioning-Induced Brain Tolerance to Ischemia

Obrenovitch¹

2008

Physiological Reviews

230

176

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Ischemic tolerance describes the adaptive biological response of cells and organs that is initiated by preconditioning (i.e., exposure to stressor of mild severity) and the associated period during which their resistance to ischemia is markedly increased. This topic is attracting much attention because preconditioning-induced ischemic tolerance is an effective experimental probe to understand how the brain protects itself. This review is focused on the molecular and related functional changes that are associated with, and may contribute to, brain ischemic tolerance. When the tolerant brain is subjected to ischemia, the resulting insult severity (i.e., residual blood flow, disruption of cellular transmembrane gradients) appears to be the same as in the naive brain, but the ensuing lesion is substantially reduced. This suggests that the adaptive changes in the tolerant brain may be primarily directed against postischemic and delayed processes that contribute to ischemic damage, but adaptive changes that are beneficial during the subsequent test insult cannot be ruled out. It has become clear that multiple effectors contribute to ischemic tolerance, including: 1) activation of fundamental cellular defense mechanisms such as antioxidant systems, heat shock proteins, and cell death/survival determinants; 2) responses at tissue level, especially reduced inflammatory responsiveness; and 3) a shift of the neuronal excitatory/inhibitory balance toward inhibition. Accordingly, an improved knowledge of preconditioning/ischemic tolerance should help us to identify neuroprotective strategies that are similar in nature to combination therapy, hence potentially capable of suppressing the multiple, parallel pathophysiological events that cause ischemic brain damage.

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Section: Sods (Mn-sod and Cu/zn-sod)mentioning

confidence: 99%

Molecular Physiology of Preconditioning-Induced Brain Tolerance to Ischemia

Obrenovitch¹

2008

Physiological Reviews

230

176

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“…A major consequence of limited nutrient availability is an alteration in the redox state in susceptible fetal tissues leading to oxidative stress. In particular, low levels of oxygen, evident in growth-retarded fetuses, will decrease the activity of complexes of the electron transport chain, which will generate increased levels of reactive oxygen species (ROS) (60)(61)(62). Overproduction of ROS initiates many oxidative reactions that lead to oxidative damage not only in the mitochondria but also in cellular proteins, lipids, and nucleic acids.…”

Section: Cellular Mechanisms: Mitochondrial Dysfunction and Oxidativementioning

confidence: 99%

“…A key adaptation enabling the fetus to survive in a limited energy environment may be the reprogramming of mitochondrial function (62)(63)(64). However, these alterations in mitochondrial function can have deleterious effects, especially in cells that have a high energy requirement, such as the ß-cell.…”

Section: Cellular Mechanisms: Mitochondrial Dysfunction and Oxidativementioning

confidence: 99%

Developmental origins of diabetes: The role of oxidative stress

Simmons

2006

Free Radical Biology and Medicine

121

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The 'thrifty phenotype' hypothesis proposes that the fetus adapts to an adverse intrauterine milieu by optimizing the use of a reduced nutrient supply to ensure survival, but by favoring the development of certain organs over that of others, this leads to persistent alterations in the growth and function of developing tissues. This concept has been somewhat controversial, however recent epidemiological, clinical, and animal studies provide support for the developmental origins of disease hypothesis. Underlying mechanisms include reprogramming of the hypothalamicpituitary-adrenal axis, islet development, and insulin signaling pathways. Emerging data suggests that oxidative stress and mitochondrial dysfunction may also play a critical role in the pathogenesis of type 2 diabetes in individuals who were growth retarded at birth.

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“…Preconditioning has been induced by mild inhibition of oxidative phosphorylation with 3-nitropropionate (Coles et al, 1979;Riepe et al, 1997a), acetylsalicylic acid (Whitehouse and Haslam, 1962;Gorgias et al, 1996;Riepe et al, 1997b) hypoxic hypoxia (Schurr et al, 1986), or heat stress (Cumming et al, 1996;Yamashita et al, 1998). Several mechanisms have been proposed to partake in preconditioning.…”

Section: Introductionmentioning

confidence: 97%

Trans‐synaptic increase of hypoxic tolerance in hippocampus upon physical challenge with two‐photon microscopy

2002

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Neuronal hypoxic tolerance is modulated by preceding challenges. We investigated hypoxic tolerance in CA1 pyramidal cells of murine hippocampal slices upon preceding physical challenge with two-photon illumination in close spatial proximity to the recorded area, at distant presynaptic neurons, or preceding chemical treatment with acetylsalicylic acid while zinc fluorescence was assessed with fluorescence measurement upon staining with N-(6-methoxy-8-quinolyl)-para-toluenesulfonamide (TSQ). Posthypoxic recovery (15 min hypoxia, 45 min recovery) of CA1 population spike amplitude (PSAP) upon stimulation of Schaffer collaterals in hippocampal region CA3 was 20 +/- 38% (mean +/- SD; n = 15) in control slices. At the end of hypoxia, zinc fluorescence increased to 120 +/- 16% (P < 0.05 to control) in slices that later recovered and 141 +/- 20% in slices that did not recover (P < 0.01 to control; P < 0.05 compared with returns). Multi-photon illumination alone was an appropriate physical challenge to improve hypoxic tolerance, even trans-synaptically. Depending on the number of illuminations posthypoxic PSAP increased up to 84 +/- 25% (P < 0.01 to control) upon illumination of hippocampal region CA1 and 85 +/- 28% (P < 0.01 to control) upon illumination of CA3. With the latter treatment, zinc fluorescence in CA1 increased to 126 +/- 20% before hypoxia (P < 0.05 to control), and no further zinc increase was observed upon subsequent hypoxia. Similar results were obtained upon chemical preconditioning with acetylsalicylate. We conclude that observation of live specimen with multi-photon imaging alters the physiology of neuronal cell ensembles, including hypoxic tolerance, even trans-synaptically at long distances from the imaged area. This is mediated in part through endogenous modulation by zinc. Mild zinc increase improves hypoxic tolerance while pronounced increase predicts neuronal cell death.

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Hypoxic pretreatment protects against neuronal damage of the rat hippocampus induced by severe hypoxia

Cited by 38 publications

References 33 publications

Molecular Physiology of Preconditioning-Induced Brain Tolerance to Ischemia

Molecular Physiology of Preconditioning-Induced Brain Tolerance to Ischemia

Developmental origins of diabetes: The role of oxidative stress

Trans‐synaptic increase of hypoxic tolerance in hippocampus upon physical challenge with two‐photon microscopy

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