Intracerebroventricular injection of naloxone blocks melatonin-dependent brain [3H]flunitrazepam binding

Gomar, María Dolores; Castillo, J. L.; Aguila, Carmen María del; Fernández, Begoña; Acuña-Castroviejo, Darı́o

doi:10.1097/00001756-199307000-00038

Cited by 28 publications

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“…A D x animals were housed under normal conditions and had free access to food and a 0.9% saline solution. At the end o f each surgical procedure indicated above, both experimental and shamoperated animals were equipped with stainless-steel cannula guides aimed at the lateral ventricle to enable central administration o f pep tides, aM T and vehicle solutions, as previously described [22]. Rats were anesthetized with equithesin (0.5-0.7 ml/rat), then positioned in a stereotaxic apparatus (David Kopft model 900, U SA ) with noninjurious ear bars.…”

Section: Methodsmentioning

confidence: 99%

“…Although the precise mechanism by which ACTH -like peptides influence plasticity is unknown, it is accepted that short A C T H fragments have no ability to release glucocorticoids in vivo and therefore act directly on the C N S [19], Neuropeptides related to A C T H may be produced by and released from neurons to act as neurotransmitters or neuromodulators, and, in addition to presynaptic events, it is also conceivable that these hormones could influence postsynaptic processes [20], In this respect, A C T H |_io has recently been reported to increase rat brain 3H-flunitrazepam (FN Z ) binding, an effect suppressed by simultaneous injection o f P-endorphin [21]. Moreover, injection o f ei ther p-endorphin or aM T increased 3H -F N Z binding to the same extent, an effect that was blocked by naloxone [22], From these data the existence o f an interaction be tween corticotropic peptides, opioids and aM T to regulate brain B N Z receptors can be assumed. Therefore, we con sidered it worthwhile to examine the relationship between aM T, A C T H |_io and A C T H 4_ io effects on cerebral cortex 3H -F N Z receptor binding in rats.…”

Section: Introductionmentioning

confidence: 99%

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Influence of the Behaviorally Active Peptides ACTH1–10, and ACTH4–10 on the Melatonin Modulation of 3H-Flunitrazepam Receptor Binding in the Rat Cerebral Cortex

Gomar

Fernández²,

Aguila³

et al. 1994

Neuroendocrinology

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Possible interactions of ACTH-like peptides with melatonin regulation of central-type benzodiazepine (BNZ) receptors have been studied by means of highaffinity ³H-fiunitrazepam binding to rat cerebral cortex membrane preparations. Intracerebroventricular injections of melatonin produce a dose-dependent increase in B_max in pinealectomized rats, without changes in K_D. Analogous effects were obtained after intracerebroventricular injection of melatonin in adrenalectomized and in adrenalectomized plus pinealectomized rats, which indicated the lack of participation of adrenal steroids in this response. Moreover, intracerebroventricular injection of ACTH_1–10 induced a similar dose-dependent increased B_max in sham-operated animals, whereas pinealectomy, but not adrenalectomy, partially counteracted this effect of ACTH_1–10 administration. Besides, simultaneous injection of ACTH_1–10 plus melatonin reverses the effects of pinealectomy, resulting in an additive effect of both compounds on B_max. The response obtained when using ACTH_4–10 was somewhat different, because no dose response was obtained in any experiment. Although lack of endogenous melatonin partially reduced the increasing effect of ACTH_4–10 on B_max, there were no additive effects at the different doses used. The results strongly suggest that ACTH-like peptides, in addition to melatonin, play a role in regulating central-type rat BNZ receptors.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Influence of the Behaviorally Active Peptides ACTH1–10, and ACTH4–10 on the Melatonin Modulation of 3H-Flunitrazepam Receptor Binding in the Rat Cerebral Cortex

Gomar

Fernández²,

Aguila³

et al. 1994

Neuroendocrinology

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“…Anticonvulsant activity of melatonin was initially shown to be related to its effects on both brain GABA-benzodiazepine receptor complex and Na + , K + -ATPase activity [103][104][105][106][107]. However, due to the inhibitory effect of melatonin on the NOS/NO system, an effect of the indoleamine on glutamate-induced excitotoxicity was soon proposed.…”

Section: Melatonin and Mitochondrial Pathologymentioning

confidence: 99%

Melatonin, Mitochondrial Homeostasis and Mitochondrial-Related Diseases

Castroviejo¹,

Escames²,

Carazo³

et al. 2002

CTMC

141

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The recently described 'hydrogen hypothesis' invokes metabolic symbiosis as the driving force for a symbiotic association between an anaerobic, strictly hydrogen-dependent organism (the host) and an eubacterium (the symbiont) that is able to respire, but which generates molecular hydrogen as an end product of anaerobic metabolism. The resulting proto-eukaryotic cell would have acquired the essentials of eukaryotic energy metabolism, evolving not only aerobic respiration, but also the cost of oxygen consumption, i.e., generation of reactive oxygen species (ROS) and oxidative damage. Mitochondria contain their own genome with a modified genetic code that is highly conserved among mammals. Control of gene expression suggests that transcription of certain mitochondrial genes may be regulated in response to the redox potential of the mitochondrial membrane. Mitochondria are involved in energy production and conservation, and they have an uncoupling mechanism to produce heat instead of ATP. Also, mitochondria are involved in programmed cell death. Increasing evidence suggests the participation of mitochondria in neurodegenerative and neuromuscular diseases involving alterations in both nuclear (nDNA) and mitochondrial (mtDNA) DNA. Melatonin is now known as a powerful antioxidant and increasing experimental evidence shows its beneficial effects against oxidative stress-induced macromolecular damage and diseases, including those in which mitochondrial function is affected. This review summarizes the data and mechanisms of action of melatonin in relation to mitochondrial pathologies.

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“…Melatonin inhibits brain excitability, regulating both g-aminobutyric acid and benzodiazepine receptors and Na þ , K þ -ATPase activity (11)(12)(13). 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).…”

Section: Introductionmentioning

confidence: 99%

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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Intracerebroventricular injection of naloxone blocks melatonin-dependent brain [3H]flunitrazepam binding

Cited by 28 publications

References 0 publications

Influence of the Behaviorally Active Peptides ACTH<sub>1–10</sub>, and ACTH<sub>4–10</sub> on the Melatonin Modulation of <sup>3</sup>H-Flunitrazepam Receptor Binding in the Rat Cerebral Cortex

Influence of the Behaviorally Active Peptides ACTH<sub>1–10</sub>, and ACTH<sub>4–10</sub> on the Melatonin Modulation of <sup>3</sup>H-Flunitrazepam Receptor Binding in the Rat Cerebral Cortex

Melatonin, Mitochondrial Homeostasis and Mitochondrial-Related Diseases

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

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