Neuroprotection by melatonin from kainate‐induced excitotoxicity in rats

Giusti, Pietro; Lipartiti, Maria; Franceschini, Davide; Schiavo, Nicola; Floreani, Maura; Manev, Hari

doi:10.1096/fasebj.10.8.8666166

Cited by 154 publications

(103 citation statements)

References 3 publications

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“…A relationship between melatonin, corticotrophic and opioid peptides and brain benzodiazepine receptors has been also reported (14,15). Recent studies have shown the ability of melatonin to counteract both kainate-and N-methyl-D-aspartate (NMDA)-induced excitotoxicity (16)(17)(18). Inhibition of the NMDA receptor activity by melatonin depends, at least partially, on its effect to reduce nitric oxide synthase activity, thus decreasing the amount of nitric oxide produced by the NMDA activation (19).…”

Section: Introductionmentioning

confidence: 96%

Comparison between tryptophan methoxyindole and kynurenine metabolic pathways in normal and preterm neonates and in neonates with acute fetal distress

Muñóz-Hoyos

Molina-Carballo²,

Macías³

et al. 1998

European Journal of Endocrinology

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Objective: To analyze the kynurenine and methoxyindole metabolic pathways of tryptophan in order to identify changes in premature neonates and in neonates suffering from fetal distress. Methods: One hundred and twelve neonates were assigned to three groups: normal neonates (control group), preterm neonates (neonates born before the 37th gestational week) and neonates suffering from fetal distress. Each of these groups was then divided in two subgroups according to the time of birth corresponding with the time of blood sampling: a diurnal subgroup, comprising neonates whose blood was sampled between 0900 and 2100 h, and a nocturnal subgroup, comprising neonates whose blood was sampled between 2100 and 0900 h. Blood samples from the umbilical artery and vein were taken in the delivery room at birth from each neonate for measurement of melatonin, the main methoxyindole pathway metabolite. Urine samples were collected from 0900 to 2100 h (diurnal groups) and from 2100 to 0900 h (nocturnal groups), and the presence of kynurenic acid, xanturenic acid, 3-hydroxyantranilic acid, L-kynurenine and 3-hydroxykynurenine determined. Results:The results show the existence of diurnal/nocturnal differences in the concentration of melatonin in cord blood and in the urinary excretion of kynurenines. In normal neonates, the production of methoxyindoles (determined as melatonin) is decreased during the day and increases at night, whereas production of kynurenines is high during the day, decreasing at night. In the fetal distress group, a significant increase in the umbilical artery concentration of melatonin was found. This group also showed a reduction in L-kynurenine concentrations in the diurnal and nocturnal groups, and an increase in xanturenic acid and 3-hydroxyantranilic acid during the day. Correlation and regression studies confirmed that the differences in the day/night pattern of the tryptophan metabolic pathways were greater in normal neonates than in the preterm and fetal distress groups. Conclusions:The results indicate the existence of an imbalance in tryptophan metabolites in preterm infants and those with fetal distress, blunting the normal diurnal/nocturnal rhythm of both melatonin and kynurenines. European Journal of Endocrinology 139 89-95

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Section: Introductionmentioning

confidence: 96%

Comparison between tryptophan methoxyindole and kynurenine metabolic pathways in normal and preterm neonates and in neonates with acute fetal distress

Muñóz-Hoyos

Molina-Carballo²,

Macías³

et al. 1998

European Journal of Endocrinology

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“…Administration of glutamate receptor agonists is a commonly used method to investigate activity-dependent events in the CNS, such as neural apoptosis, synaptic plasticity, and neurogenesis in the hippocampus [14][15][16]. For example, administration of KA induces neuronal apoptosis in pyramidal neurons in the CA1-3 region [14].…”

Section: Discussionmentioning

confidence: 99%

“…For example, administration of KA induces neuronal apoptosis in pyramidal neurons in the CA1-3 region [14]. KA administration is also known to cause mossy fiber sprouting and up-regulation of KA receptor density that consequently leads to the modification of glutaminergic synaptic transmission in the hippocampus [16].…”

Section: Discussionmentioning

confidence: 99%

Activity-dependent regulation of BRINP family genes

Motomiya

Kobayashi

Iwasaki

et al. 2007

Biochemical and Biophysical Research Communications

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We previously identified a family of novel developmentally regulated genes: BRINP1, 2, and 3, which are predominantly and widely expressed in the CNS from earlier developmental stages to adulthood. In the present study, we investigated the activity-dependent regulation of BRINP expression in the CNS. Among the three BRINP genes, BRINP1-mRNA was specifically up-regulated in the dentate gyrus of mouse hippocampus by kainic acid treatment.In cultured hippocampal neurons, the induction of BRINP1-mRNA was also observed by the activation of glutamate receptors. Although BDNF-mRNA is up-regulated in a similar activity-dependent manner, BDNF itself did not induce BRINP1-mRNA. From these results, the physiological roles of the activity-dependent induction of BRINP1-mRNA are discussed.

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“…Some of the most toxic agents which have been utilized and shown to be counteracted by melatonin include the excitatory neurotransmitter analogue kainic acid (71)(72)(73), H202 (74,75), potassium cyanide (76), lipopolysaccharide (60,77,78), hydrophobic bile acids (79), carbon tetrachloride (61), and the carcinogen safrole (63,64). Also, the damage caused by a physical agent, i.e., ionizing radiation (65,80), and a highly destructive experimental procedure known to generate free radicals, i.e., induced ischemia followed by reperfusion (81)(82)(83), has been shown to be reduced by concurrent melatonin administration.…”

Section: Melatonin As An Antioxidantmentioning

confidence: 99%

Aging and oxygen toxicity: Relation to changes in melatonin

Reíter

1997

AGE

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Melatonin (N-acetyl-5-methoxytryptamine) is a chemical mediator produced in the pineal gland and other sites in the body. The melatonin found in the blood is derived almost exclusively from the pineal gland. Since the pineal synthesizes melatonin primarily at night, blood levels of the indole are also higher at night (5-15 fold) than during the day. Some individuals on a nightly basis produce twice as much melatonin as others of the same age. Throughout life, the melatonin rhythm gradually wanes such that, in advanced age, melatonin production is usually at a minimum. Melatonin was recently found to be a free radical scavenger and antioxidant. It has been shown, in the experimental setting, to protect against both free radical induced DNA damage and oxidative stress-mediated lipid peroxidation. Pharmacologically, melatonin has been shown to reduce oxidative damage caused by such toxins as the chemical carcinogen safrole, carbon tetrachloride, paraquat, bacterial lipopolysaccharide, kainic acid, 8-aminolevulinic and amyloid 13 peptide of AIzheimer's disease as well as a model of Parkinson's disease involving the drug 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Additionally, the oxidative damage caused by agents such as ionizing radiation and excessive exercise is reduced by melatonin. Since free radical-induced molecular injury may play a significant role in aging, melatonin's ability to protect against it suggests a potential function of melatonin in deferring aging and agerelated, free radical-based diseases. Besides its ability to abate oxidative damage, other beneficial features of melatonin may be important in combating the signs of aging; these include melatonin's immune-stimulating function, its sleep-promoting ability, its function as an anti-viral agent, and general protective actions at the cellular level. Definitive tests of the specific functions of physiological levels of melatonin in processes of aging are currently being conducted.

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Neuroprotection by melatonin from kainate‐induced excitotoxicity in rats

Cited by 154 publications

References 3 publications

Comparison between tryptophan methoxyindole and kynurenine metabolic pathways in normal and preterm neonates and in neonates with acute fetal distress

Comparison between tryptophan methoxyindole and kynurenine metabolic pathways in normal and preterm neonates and in neonates with acute fetal distress

Activity-dependent regulation of BRINP family genes

Aging and oxygen toxicity: Relation to changes in melatonin

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