Comparative Effects of Magnesium Chloride and MK-801 on Infarct Volume after MCA Occlusion in Fischer-344 Rats

Pinard, Elisabeth; Izumi, Yoshikazu; Roussel, Simon; Seylaz, Jacques

doi:10.1007/978-1-4615-3452-5_15

Cited by 2 publications

(2 citation statements)

References 18 publications

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“…Energy compromised and over-stimulated neurons are efficiently protected by the administration of magnesium salts. This naturally occurring, endogenous cation protects against the detrimental actions of stress, aging, and excitotoxins, and, therefore, magnesium supplementation has been recommended for the elderly [Seelig, 1983;Landfield and Morgan, 1984;Classen et al, 1987;Wolf et al, 1990Wolf et al, , 1991Pinard et al, 1992;Fischer et al, 19931.…”

Section: Glutamate Release Calcium Overload and Hydroxyl Radical Fomentioning

confidence: 99%

“…It has already been demonstrated that magnesium and melatonin prevent overstimulation of neurons and it is remarkable that natural endogenously-occurring compounds exhibit pharmacological profiles similar to that of synthetic inhibitors of glutamate release such as riluzole. These substances exert anticonvulsant, anxiolytic, analgetic, hypnotic, and neuroprotective properties, and share anti-stress and sleeppromoting activity [Seelig, 1983;Landfield and Morgan, 1984;Classen et al, 1987;Marani and Rietveld, 1987;Scholz, 1988;Naranjo-Rodriguez et al, 1991;Pierpaoli et al, 1991;Wolf et al, 1990Wolf et al, , 1991Miller, 1992;Cheramy et al, 1992;Pinard et al, 1992;Reiter, 1992;Fischer et al, 1993;Reiter et al , 19931. Magnesium administration stimulates nocturnal melatonin formation in the pineal gland [Namboodiri et al , 1979;Morton and James, 1985;Morton, 1989;Zhao and Touitou, 19931 and can even prevent the glutamate-mediated suppression of melatonin synthesis and secretion exerted by low intensities of red light [Govitrapong and Ebadi, 1988;Meijer et al, 1993; B. Poeggeler, R.J. Reiter, D.-X.…”

Section: Glutamate and Melatonin: Two Antagonistic Neurornediatorsmentioning

confidence: 99%

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Melatonin, hydroxyl radical‐mediated oxidative damage, and aging: A hypothesis

Pöeggeler

Reíter

Tan

et al. 1993

Journal of Pineal Research

466

339

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Melatonin is a very potent and efficient endogenous radical scavenger. The pineal indolamine reacts with the highly toxic hydroxyl radical and provides on-site protection against oxidative damage to biomolecules within every cellular compartment. Melatonin acts as a primary non-enzymatic antioxidative defense against the devastating actions of the extremely reactive hydroxyl radical. Melatonin and structurally related tryptophan metabolites are evolutionary conservative molecules principally involved in the prevention of oxidative stress in organisms as different as algae and rats. The rate of aging and the time of onset of age-related diseases in rodents can be retarded by the administration of melatonin or treatments that preserve the endogenous rhythm of melatonin formation. The release of excitatory amino acids such as glutamate enhances endogenous hydroxyl radical formation. The activation of central excitatory amino acid receptors suppress melatonin synthesis and is therefore accompanied by a reduced detoxification rate of hydroxyl radicals. Aged animals and humans are melatonin-deficient and more sensitive to oxidative stress. Experiments investigating the effects of endogenous excitatory amino acid antagonists and stimulants of melatonin biosynthesis such as magnesium may finally lead to novel therapeutic approaches for the prevention of degeneration and dysdifferentiation associated with diseases related to premature aging.

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Section: Glutamate Release Calcium Overload and Hydroxyl Radical Fomentioning

confidence: 99%

Section: Glutamate and Melatonin: Two Antagonistic Neurornediatorsmentioning

confidence: 99%

Melatonin, hydroxyl radical‐mediated oxidative damage, and aging: A hypothesis

Pöeggeler

Reíter

Tan

et al. 1993

Journal of Pineal Research

466

339

View full text Add to dashboard Cite

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The Rationale for Glutamate Antagonists in the Treatment of Traumatic Brain Injury

Myseros¹,

Bullock²

1995

Annals of the New York Academy of Sciences

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The recent development of potent antagonists for the most widespread neurotransmitter in the mammalian brain has opened up possibilities for many forms of therapy. The excitotoxic hypothesis implicates excessive release of excitatory amino acids (EAAs) as an important cause of brain damage, especially in acute ischemia, and chronic neurodegeneration. Focal ischemic damage and diffuse axonal injury are the major causes of brain damage after traumatic human brain injury. Evidence from animal models has shown that excitatory amino acid-induced events maybe responsible for a proportion of the posttraumatic sequelae and that these effects can be blocked by EAA antagonists. This evidence is reviewed, and the implications for human pathophysiology and treatment are discussed.

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Comparative Effects of Magnesium Chloride and MK-801 on Infarct Volume after MCA Occlusion in Fischer-344 Rats

Cited by 2 publications

References 18 publications

Melatonin, hydroxyl radical‐mediated oxidative damage, and aging: A hypothesis

Melatonin, hydroxyl radical‐mediated oxidative damage, and aging: A hypothesis

The Rationale for Glutamate Antagonists in the Treatment of Traumatic Brain Injury

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