Involvement of excitatory neurotransmitters in the damage produced in chick embryo retinas by anoxia and extracellular high potassium

David, P.; Lusky, Moshe; Teichberg, Vivian I.

doi:10.1016/s0014-4835(88)80054-x

Cited by 64 publications

(28 citation statements)

References 19 publications

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“…Reactive oxygen species (ROS) trigger ischemic cell damage and lead to the hypersecretion of glutamate and aspartate. 1 These excess amounts of glutamate that are produced during pathologic conditions such as hypoxia 2 and ischemia-reperfusion 3,4 can ultimately lead to neuronal cell toxicity. In fact, the excess amount of glutamate that is produced during ischemiareperfusion stimulates N-methyl-D-aspartate (NMDA), which is a subtype of the glutamate receptor, 3 thereby inducing an influx of excess Ca 2þ via the NMDA receptor-operated channels.…”

Section: Methodsmentioning

confidence: 99%

Neuroprotective Effects of Angiotensin II Type 1 Receptor (AT1-R) Blocker via Modulating AT1-R Signaling and Decreased Extracellular Glutamate Levels

Fujita

Hirooka

Nakamura³

et al. 2012

Invest. Ophthalmol. Vis. Sci.

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PURPOSE.To investigate the mechanism of the neuroprotective effects of the angiotensin II type 1 receptor (AT1-R) blocker against retinal ischemia-reperfusion injury in the rat. METHODS.Retinal ischemia was induced by increasing intraocular pressure. Glutamate release from the rat retina and intravitreal PO 2 (partial pressure of oxygen) profiles were monitored during and after ischemia using a microdialysis biosensor and oxygen-sensitive microelectrodes. ELISA was used to measure changes in the expression of AT1-R. Retinal mRNA expressions of p47phox and p67phox were measured by real-time polymerase chain reaction. Reactive oxygen species (ROS) were measured using dihydroethidium.RESULTS. Administration of candesartan, which is an AT1-R blocker (ARB), suppressed ischemia-induced increases in the extracellular glutamate. Candesartan also attenuated the increase in intravitreal PO 2 during reperfusion. AT1-R expression peaked at 12 hours after reperfusion. Although there was an increase in the retinal mRNA expression of p47phox and p64phox at 12 hours after the reperfusion, administration of candesartan suppressed these expressions. The production of ROS that was detected at 12 hours after reperfusion was also suppressed by the administration of candesartan or apocynin.CONCLUSIONS. NADPH oxidase-mediated ROS production increased at 12 hours after reperfusion. Candesartan may protect neurons by decreasing extracellular glutamate immediately after reperfusion and by attenuating oxidative stress via a modulation of the AT1-R signaling that occurs during ischemic insult. (Invest Ophthalmol Vis Sci. 2012;53:4099-4110)

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Section: Methodsmentioning

confidence: 99%

Neuroprotective Effects of Angiotensin II Type 1 Receptor (AT1-R) Blocker via Modulating AT1-R Signaling and Decreased Extracellular Glutamate Levels

Fujita

Hirooka

Nakamura³

et al. 2012

Invest. Ophthalmol. Vis. Sci.

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“…However, stimulation of some of the glutamate receptors by an excess amount of glutamate under pathologic conditions such as hypoxia (6) and ischemia-reperfusion (1) is toxic to neuronal cells. The activation of the Nmethyl-D-aspartate (NMDA) receptor, a subtype of the glutamate receptor (7,8), followed by excess Ca 2+ influx via NMDA receptor-operated channels is thought to be involved in the predominant mechanism of neuronal excitotoxicity.…”

Section: Introductionmentioning

confidence: 99%

Histological Protection by Donepezil Against Neurodegeneration Induced by Ischemia–Reperfusion in the Rat Retina

et al. 2010

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Abstract. Although a blockade of acetylcholine esterase has been reported to suppress neuronal cell death induced by exogenous glutamate and β -amyloid, information is still limited regarding the neuroprotective effects of the acetylcholine esterase inhibitor donepezil. We histologically examined the effects of donepezil on neuronal injury induced by ischemia-reperfusion. Intravenous and intravitreous treatment with donepezil 15 min prior to ischemia dramatically reduced the retinal damage. The protective effect of donepezil in the ganglion cell layer was not affected by mecamylamine, a nicotinic acetylcholine-receptor antagonist, nor scopolamine, a muscarinic acetylcholine-receptor antagonist. The protective effect of donepezil in the inner plexiform layer was reduced not by mecamylamine, but by scopolamine. Neostigmine, a choline-esterase inhibitor, and pilocarpine, a muscarinic acetylcholine-receptor agonist, have protective effects in the inner plexiform layer and the inner nuclear layer. These results suggest that not only the activation of acetylcholine receptors but also a mechanism unrelated to acetylcholine-esterase inhibition contribute to the protective effect of donepezil on the ganglion cells in the ischemic-reperfused rat retina. Donepezil may be useful as a therapeutic drug against retinal diseases that cause neuronal cell death such as glaucoma with high intraocular pressure.

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“…Although in vitro methods provide in teresting insights into protection against hy poxic damage [1,2], the efficacy of a new treat ment will ultimately have to be evaluated in animal models.…”

Section: Introductionmentioning

confidence: 99%

Pressure-Induced Retinal Ischemia in Rats: An Experimental Model for Quantitative Study

1991

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The advent of treatment modalities with the potential to ameliorate retinal ischemic injury calls for methods allowing their quantitative assessment. We thus established a model of pressure-induced retinal ischemia/reperfusion injury in rats. The intraocular pressure (IOP) was raised to 110 mm Hg by cannulation of the anterior chamber for a duration of 0, 90 or 120 min. The eyes were reperfused for 3 or 7 days. Morphologically, retinal injury occurred in a pattern consistent with retinal and choroidal vascular occlusion. Damage increased in severity with prolonged durations of ischemia. Morphometric determination of the mean thickness of inner retinal layers (MTIRL) revealed significant differences between controls and the 90- or 120-min ischemia groups (p < 0.05 and p < 0.01, respectively). The difference in MTIRL between 3 and 7 days of reperfusion was not significant. Replacement of normal saline by a solution of 5% dextrose in the hydrostatic device used to increase the IOP led to a decrease in retinal injury after 120 min of ischemia (p < 0.01). This model combines a relatively simple methodology, cost-effective execution and a fast, semicomputerized method of quantitation. Depletion of carbohydrates during ischemia may contribute to retinal injury in this model.

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Involvement of excitatory neurotransmitters in the damage produced in chick embryo retinas by anoxia and extracellular high potassium

Cited by 64 publications

References 19 publications

Neuroprotective Effects of Angiotensin II Type 1 Receptor (AT1-R) Blocker via Modulating AT1-R Signaling and Decreased Extracellular Glutamate Levels

Neuroprotective Effects of Angiotensin II Type 1 Receptor (AT1-R) Blocker via Modulating AT1-R Signaling and Decreased Extracellular Glutamate Levels

Histological Protection by Donepezil Against Neurodegeneration Induced by Ischemia–Reperfusion in the Rat Retina

Pressure-Induced Retinal Ischemia in Rats: An Experimental Model for Quantitative Study

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