Ionotropic glutamate receptors and glutamate transporters are involved in necrotic neuronal cell death induced by oxygen–glucose deprivation of hippocampal slice cultures

Bonde, Christian; Noraberg, Jens; Noer, Helle; Zimmer, Jens

doi:10.1016/j.neuroscience.2005.07.020

Cited by 95 publications

(78 citation statements)

References 95 publications

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“…Activation of NMDA receptors plays a role in neuronal death induced by transient OGD in different neuronal culture systems (Martinez-Sanchez et al, 2004;Bonde et al, 2005;Ahlgren et al, 2011;Caldeira et al, 2013), similarly to the role of glutamate receptors in neuronal damage in the ischemic brain [for review (Kostandy, 2012)]. The activation of NMDA-type glutamate receptors is likely to be a mediator in OGD and ischemia-induced downregulation of the proteasome activity, as shown in experiments where cultured hippocampal neurons were subjected to excitotoxic stimulation with glutamate or with NMDA (Caldeira et al, 2013).…”

Section: Ups In Glutamate-induced Excitotoxicitymentioning

confidence: 99%

Role of the ubiquitin–proteasome system in brain ischemia: Friend or foe?

Caldeira

Salazar

Curcio

et al. 2014

Progress in Neurobiology

117

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A B S T R A C TThe ubiquitin-proteasome system (UPS) is a catalytic machinery that targets numerous cellular proteins for degradation, thus being essential to control a wide range of basic cellular processes and cell survival. Degradation of intracellular proteins via the UPS is a tightly regulated process initiated by tagging a target protein with a specific ubiquitin chain. Neurons are particularly vulnerable to any change in protein composition, and therefore the UPS is a key regulator of neuronal physiology. Alterations in UPS activity may induce pathological responses, ultimately leading to neuronal cell death. Brain ischemia triggers a complex series of biochemical and molecular mechanisms, such as an inflammatory response, an exacerbated production of misfolded and oxidized proteins, due to oxidative stress, and the breakdown of cellular integrity mainly mediated by excitotoxic glutamatergic signaling. Brain ischemia also damages protein degradation pathways which, together with the overproduction of damaged proteins and consequent upregulation of ubiquitin-conjugated proteins, contribute to the accumulation of ubiquitincontaining proteinaceous deposits. Despite recent advances, the factors leading to deposition of such aggregates after cerebral ischemic injury remain poorly understood. This review discusses the current knowledge on the role of the UPS in brain function and the molecular mechanisms contributing to UPS dysfunction in brain ischemia with consequent accumulation of ubiquitin-containing proteins. Chemical inhibitors of the proteasome and small molecule inhibitors of deubiquitinating enzymes, which promote the degradation of proteins by the proteasome, were both shown to provide neuroprotection in brain ischemia, and this apparent contradiction is also discussed in this review. ß

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Section: Ups In Glutamate-induced Excitotoxicitymentioning

confidence: 99%

Role of the ubiquitin–proteasome system in brain ischemia: Friend or foe?

Caldeira

Salazar

Curcio

et al. 2014

Progress in Neurobiology

117

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“…Glutamate is one of the most widespread excitatory neurotransmitters in the brain. In small amounts, it is indispensable for neuronal function, while in excessive amounts it is a neuronal poison (excitotoxin) that stimulates Ca 2+ influx into neurons (Liljequist et al 1995;Bonde et al 2005). If the excessive extracellular release of glutamate is not regulated, it could lead to brain damage (Robinson 2006).…”

Section: Stimulation Of Glutamate Activation Of Nmda and Ampa Receptmentioning

confidence: 99%

Physiological Neuroprotective Mechanisms in Natural Genetic Systems: Therapeutic Clues for Hypoxia-Induced Brain Injuries

Nathaniel¹,

Umesiri²,

Reifler³

et al. 2012

Brain Injury - Pathogenesis, Monitoring, Recovery and Management

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“…These are important components of several pharmacologically active compounds [2][3][4][5][6][7][8] and exhibit special and wider ranges of functions in biologically active compounds [9], electroluminescent materials [10], dyes [11] and anion sensors [12]. Although rarely describe in nature, synthetic quinoxaline derivatives showed variety of pharmaceutical activities encompassed major types of drug target families and effective in many clinical applications such as anti tumor agents [13], kinase inhibitors [14], HIV drugs [15], antibiotics [16], ion channel regulators [17] and anti protozoal agents [18].…”

Section: Introductionmentioning

confidence: 99%

Synthesis of Thiophenyl Thiazole Based Novel Quinoxaline Derivatives

Kathrotiya

Naliapara

2015

ILCPA

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A new series of thiophenyl thiazole based novel quinoxaline derivatives 4a-4t have been synthesized by base catalysed condensation reaction. In which 6-substituted 2,3-dichloroquinoxaline 1a and 4-(thiophen-2-yl)thiazol-2-amine 2b reacted in basic condition to afford intermediate 3c which reacts with various aromatic amine to form final compounds. Easy experimental procedure, high yield, and selectivity are the imperative features of this method. The identity of all the compounds has been established by 1 H NMR, 13 C NMR, FT-IR, and elemental analysis.

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Ionotropic glutamate receptors and glutamate transporters are involved in necrotic neuronal cell death induced by oxygen–glucose deprivation of hippocampal slice cultures

Cited by 95 publications

References 95 publications

Role of the ubiquitin–proteasome system in brain ischemia: Friend or foe?

Role of the ubiquitin–proteasome system in brain ischemia: Friend or foe?

Physiological Neuroprotective Mechanisms in Natural Genetic Systems: Therapeutic Clues for Hypoxia-Induced Brain Injuries

Synthesis of Thiophenyl Thiazole Based Novel Quinoxaline Derivatives

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