Journal ArticleDOI
Ca2+ influx through glutamate receptor-associated channels in retina cells correlates with neuronal cell death
TLDR
The results show that the activation of NMDA or AMPA/kainate receptors can cause excitotoxicity in retinal neurons by mechanisms not involving Na+ influx, but rather depending on the permeation of Ca2+ through glutamate receptor-associated channels.About:
This article is published in European Journal of Pharmacology.The article was published on 1996-04-29. It has received 75 citations till now. The article focuses on the topics: Kainate receptor & Kainic acid.read more
Citations
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Journal ArticleDOI
Retinal ischemia: mechanisms of damage and potential therapeutic strategies.
TL;DR: Given the increasing understanding of the events involved in ischemic neuronal injury, it is hoped that clinically effective treatments for retinal ischemia will soon be available.
Journal ArticleDOI
Diversity of glutamate receptors in the mammalian retina
TL;DR: This article will concentrate on glutamate receptors with the intention of reviewing some of the recent data on glutamate receptor expression in the mammalian retina and their possible involvement in retinal function.
Book ChapterDOI
Review of the Biological and Health Effects of Aflatoxins on Body Organs and Body Systems
Godfrey S. Bbosa,David Kitya,Aloysius Lubega,Jasper Ogwal-Okeng,William W. Anokbonggo,David B. Kyegombe +5 more
TL;DR: The aflatoxins were initially isolated and identified as the causative agent in Turkey X disease that caused necrosis of the liver in 1960 and over 100,000 turkeys died in England and USA and the death was attributed to a mould-contaminated peanut meal.
Journal ArticleDOI
In vivo and in vitro experiments show that betaxolol is a retinal neuroprotective agent.
TL;DR: The combined data show that betaxolol is a neuroprotective agent and attenuates the effects on the retina induced by raising the intraocular pressure to simulate an ischaemic insult as may occur in glaucoma.
Journal ArticleDOI
Role of the ubiquitin–proteasome system in brain ischemia: Friend or foe?
Margarida V. Caldeira,Ivan L. Salazar,Michele Curcio,Lorella M.T. Canzoniero,Carlos B. Duarte +4 more
TL;DR: 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 are discussed.
References
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Journal ArticleDOI
Rapid colorimetric assay for cellular growth and survival: Application to proliferation and cytotoxicity assays
TL;DR: A tetrazolium salt has been used to develop a quantitative colorimetric assay for mammalian cell survival and proliferation and is used to measure proliferative lymphokines, mitogen stimulations and complement-mediated lysis.
Journal ArticleDOI
Magnesium gates glutamate-activated channels in mouse central neurones
TL;DR: The voltage dependence of the NMDA receptor-linked conductance appears to be a consequence of the voltage dependenceof the Mg2+ block and its interpretation does not require the implication of an intramembrane voltage-dependent ‘gate’.
Journal ArticleDOI
Glycine potentiates the NMDA response in cultured mouse brain neurons
J. W. Johnson,P Ascher +1 more
TL;DR: G glycine may facilitate excitatory transmission in the brain through an allosteric activation of the NMDA receptor, and can be observed in outside-out patches as an increase in the frequency of opening of the channels activated by NMDA agonists.
Journal ArticleDOI
The role of glutamate neurotoxicity in hypoxic- ischemic neuronal death
Dennis W. Choi,Steven M. Rothman +1 more
TL;DR: A critical question has been why brain, more than mostother tissues, is so vulnerable to hypoxic-ischemic insults, and at least some of this special vulnerability may be accounted for by the central neurotoxicity of the endogenous excitatory
Journal ArticleDOI
Excitatory amino acid neurotoxicity and neurodegenerative disease
Brian S. Meldrum,John Garthwaite +1 more
TL;DR: In vivo and in vitro studies of the cytotoxicity of amino acids are reviewed and the contribution of such toxicity to acute and chronic neurodegenerative disorders is summarized.