scholarly journals Aerobic production and utilization of lactate satisfy increased energy demands upon neuronal activation in hippocampal slices and provide neuroprotection against oxidative stress

2011 ◽  
Author(s):  
Schurr
Keyword(s):  
Oxidative Stress ◽  
Hippocampal Slices ◽  
Neuronal Activation ◽  
Energy Demands

Guanosine enhances glutamate uptake and oxidation, preventing oxidative stress in mouse hippocampal slices submitted to high glutamate levels

2020 ◽  
Vol 1748 ◽  
pp. 147080
Author(s):  
Y. Nonose ◽  
L.Z. Pieper ◽  
J.S. da Silva ◽  
A. Longoni ◽  
R.V. Apel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Glutamate Uptake ◽  
Hippocampal Slices

Neuroprotective effects of arachidonic acid against oxidative stress on rat hippocampal slices

2006 ◽  
Vol 163 (3) ◽  
pp. 207-217 ◽  
Author(s):  
Ze-Jian Wang ◽  
Cui-Ling Liang ◽  
Guang-Mei Li ◽  
Cai-Yi Yu ◽  
Ming Yin
Keyword(s):  
Oxidative Stress ◽  
Arachidonic Acid ◽  
Hippocampal Slices ◽  
Neuroprotective Effects

Trichilia catigua (Catuaba) bark extract exerts neuroprotection against oxidative stress induced by different neurotoxic agents in rat hippocampal slices

2013 ◽  
Vol 50 ◽  
pp. 625-632 ◽  
Author(s):  
Jean Paul Kamdem ◽  
Elekofehinti Olusola Olalekan ◽  
Waseem Hassan ◽  
Ige Joseph Kade ◽  
Ogunbolude Yetunde ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hippocampal Slices ◽  
Bark Extract

scholarly journals Oxidative stress mediated by NMDA, AMPA/KA channels in acute hippocampal slices: Neuroprotective effect of resveratrol

2014 ◽  
Vol 28 (4) ◽  
pp. 544-551 ◽  
Author(s):  
André Quincozes-Santos ◽  
Larissa Daniele Bobermin ◽  
Ana Carolina Tramontina ◽  
Krista Minéia Wartchow ◽  
Bárbara Tagliari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neuroprotective Effect ◽  
Hippocampal Slices ◽  
Acute Hippocampal Slices

scholarly journals Neurotoxicity of Unconjugated Bilirubin in Neonatal Hypoxic-Ischemic Brain Injury in vitro

2021 ◽  
Vol 9 ◽  
Author(s):  
Carlo Dani ◽  
Simone Pratesi ◽  
Guido Mannaioni ◽  
Elisabetta Gerace
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Preterm Infants ◽  
Neuronal Death ◽  
Hippocampal Slices ◽  
Unconjugated Bilirubin ◽  
Pharmacological Intervention ◽  
Common Mechanism ◽  
Slight Reduction

Background: The pathophysiology of bilirubin neurotoxicity in course of hypoxic–ischemic encephalopathy (HIE) in term and preterm infants is still poorly understood. We hypothesized that oxidative stress may be a common mechanism that link hyperbilirubinemia and HIE.Objectives: The objective of the present study was to evaluate whether unconjugated bilirubin (UCB) may enhance the HI brain injury by increasing oxidative stress and to test pioglitazone and allopurinol as new antioxidant therapeutic drugs in vitro.Methods: The effects of UCB were tested on organotypic hippocampal slices subjected to 30 min oxygen-glucose deprivation (OGD), used as in vitro model of HIE. The experiments were performed on mature (14 days in culture) and immature (7 days in culture) slices, to mimic the brains of term and preterm infants, respectively. Mature and immature slices were exposed to UCB, human serum albumin (HSA), pioglitazone, and/or allopurinol for 24 h, immediately after 30 min OGD. Neuronal injury was assessed using propidium iodide (PI) fluorescence. ROS formation was quantified by using the 2′,7′-dichlorodihydrofluorescein diacetate (DCF-DA) method.Results: In mature slices, we found that the neurotoxicity, as well as oxidative stress, induced by OGD were enhanced by UCB. HSA significantly prevented UCB-increased neurotoxicity, but had a slight reduction on ROS production. Allopurinol, but not pioglitazone, significantly reduced UCB-increased neurotoxicity induced by OGD. In immature slices exposed to OGD, no increase of neuronal death was observed, whereas oxidative stress was detected after UCB exposure. HSA, pioglitazone and allopurinol have no protective effects on both OGD-induced neuronal death and on UCB-induced oxidative stress. For this reason, UCB, pioglitazone and allopurinol was also tested on ischemic preconditioning protocol. We found that UCB abolished the neuroprotection induced by preconditioning and increased oxidative stress. These effects were restored by allopurinol but not pioglitazone.Conclusions: UCB characterized a different path of neuronal damage and oxidative stress in mature and immature hippocampal slice model of HIE. Management of hyperbilirubinemia in a complex pathological condition, such as HIE and hyperbilirubinemia, should be very careful. Allopurinol could deserve attention as a novel pharmacological intervention for hyperbilirubinemia and HIE.

scholarly journals The Post-Ischemic Increase in GluA2 Ser880 Phosphorylation Involves NADPH Oxidase

2018 ◽  
Vol 4 (1) ◽  
pp. 170-181
Author(s):  
Darrell A. Jackson ◽  
Fanny Astruc-Diaz ◽  
Nicole M. Byrnes ◽  
Phillip H. Beske
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Oxidase Activity ◽  
Hippocampal Slices ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Glucose Deprivation ◽  
Subunit Composition ◽  
Stress Signaling ◽  
Scaffolding Proteins ◽  
Nadph Oxidase Activity

Most 2-amino-3-(3-hydroxy-5-methyl-isoxazol-4-yl) propanoic acid receptors (AMPARs) expressed on adult hippocampal pyramidal neurons contain the edited form of GluA2 (Q607R) and are thus impermeable to Ca2+/Zn2+ entry.  Following ischemic injury, these receptors undergo a subunit composition change, switching from a GluA2-containing Ca2+/Zn2+-impermeable AMPAR to a GluA2-lacking Ca2+/Zn2+-permeable AMPAR. Recent studies indicate that an oxidative stress signaling pathway is responsible for the I/R-induced changes in AMPAR subunit composition.  Studies suggest that nicotinamide adenine dinucleotide phosphate-oxidase (NADPH oxidase), a superoxide generator, is the source that initiates the oxidative stress-signaling cascade during post-ischemic reperfusion. The objective of the present study was to determine if suppression of NADPH oxidase activity prevents the increase in phosphorylation and subsequent internalization of the GluA2 AMPAR subunit during reperfusion of post-ischemic hippocampal slices. In this study, we demonstrated that exposure of adult rat hippocampal slices to oxygen glucose deprivation/reperfusion (OGD/R) results in an increase in Ser880 phosphorylation of the GluA2 subunit.  The increase in Ser880 phosphorylation resulted in the dissociation of GluA2 from the scaffolding proteins Glutamate receptor-interacting protein 1 (GRIP1) and AMPAR binding protein (ABP), thus enabling the association of GluA2 with protein interacting with C kinase 1 (PICK1). OGD/R also resulted in an increase in the association of activated protein kinase C ? (PKC?) with PICK1. We have found that pharmacological inhibition of NADPH oxidase with apocynin diminishes the OGD/R-induced increase in activated PKC? association with PICK1 and subsequent Ser880 phosphorylation of GluA2. Suppression of NADPH oxidase activity also blunted OGD/R-induced decreased association of GluA2 with the scaffolding proteins GRIP1 and ABP.  Protein phosphatase 2A (PP2A), which regulates PKC? activity by dephosphorylating the kinase, was inactivated by OGD/R-induced increase in tyrosine phosphorylation of the phosphatase (Y307). Inhibition of NADPH oxidase activity ameliorated OGD/R-induced PP2A phosphorylation and inactivation. Our findings are consistent with a model of OGD/R-induced Ser880 phosphorylation of GluA2 that implicates NADPH oxidase mediated inactivation of PP2A and sustained PKC? phosphorylation of GluA2.

scholarly journals The Role of the Antioxidant Response in Mitochondrial Dysfunction in Degenerative Diseases: Cross-Talk between Antioxidant Defense, Autophagy, and Apoptosis

2019 ◽  
Vol 2019 ◽  
pp. 1-26 ◽  
Author(s):  
Michael L.-H. Huang ◽  
Shannon Chiang ◽  
Danuta S. Kalinowski ◽  
Dong-Hun Bae ◽  
Sumit Sahni ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Dynamics ◽  
Signal Transmission ◽  
Antioxidant Response ◽  
High Energy ◽  
Stress Factors ◽  
Degenerative Diseases ◽  
Energy Demands ◽  
Stress Energy

The mitochondrion is an essential organelle important for the generation of ATP for cellular function. This is especially critical for cells with high energy demands, such as neurons for signal transmission and cardiomyocytes for the continuous mechanical work of the heart. However, deleterious reactive oxygen species are generated as a result of mitochondrial electron transport, requiring a rigorous activation of antioxidative defense in order to maintain homeostatic mitochondrial function. Indeed, recent studies have demonstrated that the dysregulation of antioxidant response leads to mitochondrial dysfunction in human degenerative diseases affecting the nervous system and the heart. In this review, we outline and discuss the mitochondrial and oxidative stress factors causing degenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and Friedreich’s ataxia. In particular, the pathological involvement of mitochondrial dysfunction in relation to oxidative stress, energy metabolism, mitochondrial dynamics, and cell death will be explored. Understanding the pathology and the development of these diseases has highlighted novel regulators in the homeostatic maintenance of mitochondria. Importantly, this offers potential therapeutic targets in the development of future treatments for these degenerative diseases.

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