Melatonin-dopamine interaction in the striatal projection area of sensorimotor cortex in the rat

Escames, Germaine; Castroviejo, Darío Acuña; Vives, Francisco

doi:10.1097/00001756-199601310-00053

Cited by 54 publications

(46 citation statements)

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“…Besides these mechanisms, it has been recently reported that melatonin reverts 6-OHDA-induced striatal neurochemical alterations in association with striatal D 1 /D 2 DA receptor modification [6]. These data agree with he interaction between melatonin and striatal D 1 /D 2 receptors elsewhere reported with electrophysiological approaches [18]. Experiments in vivo and in vitro have shown that melatonin promotes mitochondrial phosphorylation and ATP synthesis interacting with the electron transport chain complexes I and IV [5,[37][38][39].…”

Section: Discussionsupporting

confidence: 88%

Synergistic effects of melatonin and deprenyl against MPTP-induced mitochondrial damage and DA depletion

Khaldy

Escames

León

et al. 2003

Neurobiology of Aging

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Previous studies showed a synergistic effect of melatonin and deprenyl against dopamine (DA) autoxidation in vitro. Since oxidative stress is implicated in Parkinson's disease (PD), we explored the effects of melatonin plus deprenyl administration in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD in C57/Bl6 mice. Melatonin, but not deprenyl prevents the inhibition of mitochondrial complex I and the oxidative damage in nigrostriatal neurons induced by MPTP. With the dose used deprenyl recovers 50% DA levels and tyrosine hydroxylase activity depressed by the neurotoxin, normalizing locomotor activity of mice. Melatonin, which was unable to counteract MPTP-induced DA depletion and inhibition of tyrosine hydroxylase activity, potentiates the effect of deprenyl on catecholamine turnover and mice ambulatory activity. These results suggest a dissociation of complex I inhibition from DA depletion in this model of Parkinson's disease. The data also support that a combination of melatonin, which improves mitochondrial electron transport chain and reduces oxidative damage, and deprenyl, which promotes the specific function of the rescued neurons, i.e. DA turnover, may be a promising strategy for the treatment of PD.

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Section: Discussionsupporting

confidence: 88%

Synergistic effects of melatonin and deprenyl against MPTP-induced mitochondrial damage and DA depletion

Khaldy

Escames

León

et al. 2003

Neurobiology of Aging

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“…Reduced melatonin levels are related to increased brain damage after stroke or excitotoxic seizures in rats [Manev et al, 1996], whereas melatonin protected the brain against kainic acid or quinolinic acid oxidative damage Tan et al, 1998;Cabrera et al, 2000]. Electrophysiological experiments further demonstrated the antagonism of melatonin against the NMDA-induced excitotoxicity, an effect involving the inhibition of the nNOS [Escames et al, 1996;Leó n et al, 1998Leó n et al, , 2000. Melatonin also counteracts oxidative damage in MPTP-induced Parkinson's disease [Acuñ a-Castroviejo et al, 1997], and in vitro melatonin was more potent than vitamins E and C, and L-deprenyl in blocking dopamine (DA) autoxidation .…”

Section: Melatonin and Ros And Rnsmentioning

confidence: 99%

Melatonin, mitochondria, and cellular bioenergetics

Acuña-Castroviejo

Martı́n

Macías

et al. 2001

Journal of Pineal Research

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383

313

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Aerobic cells use oxygen for the production of 90-95% of the total amount of ATP that they use. This amounts to about 40 kg ATP/day in an adult human. The synthesis of ATP via the mitochondrial respiratory chain is the result of electron transport across the electron transport chain coupled to oxidative phosphorylation. Although ideally all the oxygen should be reduced to water by a four-electron reduction reaction driven by the cytochrome oxidase, under normal conditions a small percentage of oxygen may be reduced by one, two, or three electrons only, yielding superoxide anion, hydrogen peroxide, and the hydroxyl radical, respectively. The main radical produced by mitochondria is superoxide anion and the intramitochondrial antioxidant systems should scavenge this radical to avoid oxidative damage, which leads to impaired ATP production.

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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: 95%

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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Melatonin-dopamine interaction in the striatal projection area of sensorimotor cortex in the rat

Cited by 54 publications

References 0 publications

Synergistic effects of melatonin and deprenyl against MPTP-induced mitochondrial damage and DA depletion

Synergistic effects of melatonin and deprenyl against MPTP-induced mitochondrial damage and DA depletion

Melatonin, mitochondria, and cellular bioenergetics

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

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