Glutamate receptor and transporter modifications in rat organotypic hippocampal slice cultures exposed to oxygen–glucose deprivation: The contribution of cyclooxygenase-2

Llorente, Irene L.; Landucci, Elisa; Pellegrini‐Giampietro, Domenico E.; Fernández‐López, Arsenio

doi:10.1016/j.neuroscience.2015.02.040

Cited by 13 publications

(7 citation statements)

References 48 publications

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“…In organotypic hippocampal slices subjected to an in vitro model of ischemia-reperfusion, transcript levels for EAAT1 initially dropped to be induced at later time points, while EAAT2 gene transcription was downregulated [120]. The latter observation is in line with the fact that global brain ischemia decreases EAAT2 protein levels [121].…”

Section: Regulation Of Expression Levels Of Eaatsmentioning

confidence: 95%

Excitatory Amino Acid Transporters in Physiology and Disorders of the Central Nervous System

Malik

Willnow

2019

IJMS

118

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Excitatory amino acid transporters (EAATs) encompass a class of five transporters with distinct expression in neurons and glia of the central nervous system (CNS). EAATs are mainly recognized for their role in uptake of the amino acid glutamate, the major excitatory neurotransmitter. EAATs-mediated clearance of glutamate released by neurons is vital to maintain proper glutamatergic signalling and to prevent toxic accumulation of this amino acid in the extracellular space. In addition, some EAATs also act as chloride channels or mediate the uptake of cysteine, required to produce the reactive oxygen speciesscavenger glutathione. Given their central role in glutamate homeostasis in the brain, as well as their additional activities, it comes as no surprise that EAAT dysfunctions have been implicated in numerous acute or chronic diseases of the CNS, including ischemic stroke and epilepsy, cerebellar ataxias, amyotrophic lateral sclerosis, Alzheimer’s disease and Huntington’s disease. Here we review the studies in cellular and animal models, as well as in humans that highlight the roles of EAATs in the pathogenesis of these devastating disorders. We also discuss the mechanisms regulating EAATs expression and intracellular trafficking and new exciting possibilities to modulate EAATs and to provide neuroprotection in course of pathologies affecting the CNS.

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Section: Regulation Of Expression Levels Of Eaatsmentioning

confidence: 95%

Excitatory Amino Acid Transporters in Physiology and Disorders of the Central Nervous System

Malik

Willnow

2019

IJMS

118

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“…The OGD model can be used to simulate the OGD environment observed in the process of ischemic stroke, and there are well-established procedures for using organotypic brain slice preparations as an OGD model [ 22 , 23 ]. PI, used for nuclear staining, passes through disrupted cell membranes to combine with DNA and can be detected by its bright red fluorescence.…”

Section: Discussionmentioning

confidence: 99%

Effects of Gualou Guizhi Decoction Aqueous Extract on Axonal Regeneration in Organotypic Cortical Slice Culture after Oxygen‐Glucose Deprivation

Nan

Yang²,

Zheng

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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Gualou Guizhi decoction (GLGZD) is effective for the clinical treatment of limb spasms caused by ischemic stroke, but its underlying mechanism is unclear. Propidium iodide (PI) fluorescence staining, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL), immunohistochemistry, western blot, and real-time qPCR were used to observe the axonal regeneration and neuroprotective effects of GLGZD aqueous extract on organotypic cortical slices exposed to oxygen-glucose deprivation (OGD) and further elucidate the potential mechanisms. Compared with the OGD group, the GLGZD aqueous extract decreased the red PI fluorescence intensity; inhibited neuronal apoptosis; improved the growth of slice axons; upregulated the protein expression of tau and growth-associated protein-43; and decreased protein and mRNA expression of neurite outgrowth inhibitor protein-A (Nogo-A), Nogo receptor 1 (NgR1), ras homolog gene family A (RhoA), rho-associated coiled-coil-containing protein kinase (ROCK), and phosphorylation of collapsin response mediator protein 2 (CRMP2). Our study found that GLGZD had a strong neuroprotective effect on brain slices after OGD injury. GLGZD plays a vital role in promoting axonal remodeling and functional remodeling, which may be related to regulation of the expression of Nogo-A and its receptor NgR1, near the injured axons, inhibition of the Rho-ROCK pathway, and reduction of CRMP2 phosphorylation.

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“…In a carotid embolism stroke model, atorvastatin and meloxicam reduced the inflammatory process, neurodegeneration, and morphological changes specific for astrocytes and microglia ( 124 ). Llorente et al ( 125 ) examined whether meloxicam protects against glutamatergic excitotoxicity in cultures of organotypic hippocampal slices. They found decreased mRNA synthesis of glutamatergic transporters VGLUT1, VGLUT2, GLAST-1A, GLT-1 and EAAC-1 and some receptor subunits, but not of membrane transporters.…”

Section: Experimental Evidence For Pharmacological Checkpoints Of mentioning

confidence: 99%

Neuroinflammation and microglia/macrophage phenotype modulate the molecular background of post-stroke depression: A literature review

et al. 2020

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Increasing evidence hints to the central role of neuroinflammation in the development of post-stroke depression. Danger signals released in the acute phase of ischemia trigger microglial activation, along with the infiltration of neutrophils and macrophages. The increased secretion of proinflammatory cytokines interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor α (TNFα) provokes neuronal degeneration and apoptosis, whereas IL-6, interferon γ (IFNγ), and TNFα induce aberrant tryptophane degradation with the accumulation of the end-product quinolinic acid in resident glial cells. This promotes glutamate excitotoxicity via hyperexcitation of N-methyl-D-aspartate receptors and antagonizes 5-hydroxy-tryptamine, reducing synaptic plasticity and neuronal survival, thus favoring depression. In the post-stroke period, CX3CL1 and the CD200-CD200R interaction mediates the activation of glial cells, whereas CCL-2 attracts infiltrating macrophages. CD206 positive cells grant the removal of excessive danger signals; the high number of regulatory T cells, IL-4, IL-10, transforming growth factor β (TGFβ), and intracellular signaling via cAMP response element-binding protein (CREB) support the M2 type differentiation. In favorable conditions, these cells may exert efficient clearance, mediate tissue repair, and might be essential players in the downregulation of molecular pathways that promote post-stroke depression. Contents 1. Introduction: Systemic and neuroinflammation are both characteristic in certain forms of post-stroke depression 2. Post-stroke depression, genetic factors and lesion localization 3. Brain-derived neurotrophic factor: A link between purinergic signaling, neuroinflammation and depression 4. The post-stroke immune pathways and tissue repair 5. The microglia/macrophage network in post-stroke depression 6. Mediators of neuroinflammation are key elements in the post-ischemic response 7. Experimental evidence for pharmacological checkpoints of inflammation 8. Discussion 1. Introduction: Systemic and neuroinflammation are both characteristic in certain forms of post-stroke depression Stroke is a medical emergency that frequently results in severe neurological sequelae and other complex dysfunctions. Among these, post-stroke depression (PSD) is prevalent, being

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Glutamate receptor and transporter modifications in rat organotypic hippocampal slice cultures exposed to oxygen–glucose deprivation: The contribution of cyclooxygenase-2

Cited by 13 publications

References 48 publications

Excitatory Amino Acid Transporters in Physiology and Disorders of the Central Nervous System

Excitatory Amino Acid Transporters in Physiology and Disorders of the Central Nervous System

Effects of Gualou Guizhi Decoction Aqueous Extract on Axonal Regeneration in Organotypic Cortical Slice Culture after Oxygen‐Glucose Deprivation

Neuroinflammation and microglia/macrophage phenotype modulate the molecular background of post-stroke depression: A literature review

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