Adaptation of adult brain tissue to anoxia and hypoxia in vitro

Schurr, Avital; Reid, Kenneth H.; Tseng, Michael T.; West, Catherine A.; Rigor, Benjamin M.

doi:10.1016/0006-8993(86)90418-x

Cited by 164 publications

(86 citation statements)

References 10 publications

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“…This manipulation reduces bath oxygen tension in the recording chamber from E600 to E250 mm Hg (Sebastião et al, 2000). Each slice was subjected to a single period of hypoxia, since the effects of hypoxia may be modified by subsequent episodes in the same slice (Schurr et al, 1986). To minimize individual variation between slices, the effects of hypoxia were compared in control and in test slices with less than 1 h of interval.…”

Section: Electrophysiological Recordings In Hippocampal Slice Preparamentioning

confidence: 99%

Interleukin-6 Upregulates Neuronal Adenosine A1 Receptors: Implications for Neuromodulation and Neuroprotection

Biber

Pinto-Duarte

Wittendorp

et al. 2007

Neuropsychopharmacol

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The immunological response in the brain is crucial to overcome neuropathological events. Some inflammatory mediators, such as the immunoregulatory cytokine interleukin-6 (IL-6) affect neuromodulation and may also play protective roles against various noxious conditions. However, the fundamental mechanisms underlying the long-term effects of IL-6 in the brain remain unclear. We now report that IL-6 increases the expression and function of the neuronal adenosine A 1 receptor, with relevant consequences to synaptic transmission and neuroprotection. IL-6-induced amplification of A 1 receptor function enhances the responses to readily released adenosine during hypoxia, enables neuronal rescue from glutamate-induced death, and protects animals from chemically induced convulsing seizures. Taken together, these results suggest that IL-6 minimizes the consequences of excitotoxic episodes on brain function through the enhancement of endogenous adenosinergic signaling.

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Section: Electrophysiological Recordings In Hippocampal Slice Preparamentioning

confidence: 99%

Interleukin-6 Upregulates Neuronal Adenosine A1 Receptors: Implications for Neuromodulation and Neuroprotection

Biber

Pinto-Duarte

Wittendorp

et al. 2007

Neuropsychopharmacol

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“…The phenomenon of ischemic or hypoxic preconditioning (HPC) has been well documented in the heart and the brain [3][4][5][6] .…”

Section: Introductionmentioning

confidence: 99%

Hypoxic preconditioning in an autohypoxic animal model

Shao

2012

Neurosci. Bull.

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Abstract:Hypoxic preconditioning refers to the exposure of organisms, systems, organs, tissues or cells to moderate hypoxia/ischemia that results in increased resistance to a subsequent episode of severe hypoxia/ischemia. In this article, we review recent research based on a mouse model of repeated exposure to autohypoxia. Pre-exposure markedly increases the tolerance to or protection against hypoxic insult, and preserves the cellular structure of the brain. Furthermore, the hippocampal activity amplitude and frequency of electroencephalogram, latency of cortical somatosensory-evoked potential and spinal somatosensory-evoked potential progressively decrease, while spatial learning and memory improve. In the brain, detrimental neurochemicals such as free radicals are down-regulated, while beneficial ones such as adenosine are upregulated. Also, antihypoxia factor(s) and gene(s) are activated. We propose that the tolerance and protective effects depend on energy conservation and plasticity triggered by exposure to hypoxia via oxygen-sensing transduction pathways and hypoxia-inducible factor-initiated cascades. A potential path for further research is the development of devices and pharmaceuticals acting on antihypoxia factor(s) and gene(s) for the prevention and treatment of hypoxia and related syndromes.

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“…This neuroprotection is believed to occur through complex signal transduction pathways involving the activations of adenosine receptors [8,9] , protein kinase C [10][11][12][13] and mitochondrial adenosine triphosphate-regulated potassium (K ATP ) channels [2,14] . Interestingly, the effect of ischemic preconditioning (IPC) of brain [15,16] was demonstrated before that of heart IPC [17] . Brain and heart share common signal transduction pathways, including activation of K ATP channel [18,19] .…”

Section: Introductionmentioning

confidence: 99%

Duplicate preconditioning with sevoflurane in vitro improves neuroprotection in rat brain via activating the extracellular signal-regulated protein kinase

et al. 2010

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Abstract:Objective Sevoflurane preconditioning has been demonstrated to reduce cerebral ischemia-reperfusion (IR) injury, but the underlying mechanisms have not been fully elucidated. Besides, different protocols would usually lead to different results. The objective of this study was to determine whether dual exposure to sevoflurane improves the effect of anesthetic preconditioning against oxygen and glucose deprivation (OGD) injury in vitro. Methods Rat hippocampal slices under normoxic conditions (95% O 2 /5% CO 2 ) were pre-exposed to sevoflurane 1, 2 and 3 minimum alveolar concentration (MAC) for 30 min, once or twice, with 15-min washout after each exposure. The slices were then subjected to 13-min OGD treatment (95% N 2 /5% CO 2 , glucose-free), followed by 30-min reoxygenation. The population spikes (PSs) were recorded in the CA1 region of rat hippocampus. The percentage of PS amplitude at the end of 30-min reoxygenation to that before OGD treatment was calculated, since it could indicate the recovery degree of neuronal function. In addition, to assess the role of mitogen-activated protein kinases (MAPKs) in preconditioning, U0126, an inhibitor of extracellular signal-regulated protein kinase (MEK-ERK1/2, ERK1/2 MAPK), and SB203580, an inhibitor of p38 MAPK, were separately added 10 min before sevoflurane exposure. Results Preconditioning once with sevoflurane 1, 2, and 3 MAC increased the percentage of PS amplitude at the end of 30-min reoxygenation to that before OGD treatment, from (15.13±3.79)% (control) to (31.88±5.36)%, (44.00±5.01)%, and (49.50±6.25)%, respectively, and twice preconditioning with sevoflurane 1, 2, and 3 MAC increased the percentage to (38.53±4.36)%, (50.74±7.05)% and (55.86±6.23)%, respectively. The effect of duplicate preconditioning with sevoflurane 3 MAC was blocked by U0126 [(16.23±4.62)%]. Conclusion Sevoflurane preconditioning can induce neuroprotection against OGD injury in vitro, and preconditioning twice enhances this effect. Besides, the activation of extracellular signal-regulated protein kinase (MEK-ERK1/2, ERK1/2 MAPK) may be involved in this process.

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Adaptation of adult brain tissue to anoxia and hypoxia in vitro

Cited by 164 publications

References 10 publications

Interleukin-6 Upregulates Neuronal Adenosine A1 Receptors: Implications for Neuromodulation and Neuroprotection

Interleukin-6 Upregulates Neuronal Adenosine A1 Receptors: Implications for Neuromodulation and Neuroprotection

Hypoxic preconditioning in an autohypoxic animal model

Duplicate preconditioning with sevoflurane in vitro improves neuroprotection in rat brain via activating the extracellular signal-regulated protein kinase

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