Involvement of melatonin metabolites in the long-term inhibitory effect of the hormone on rat spinal nociceptive transmission

Mondaca, Mauricio; Hernández, Alejandro; Valladares, Luis; Sierralta, Walter; Noseda, Rodrigo; Soto-Moyano, Rubén

doi:10.1016/j.pbb.2003.11.007

Cited by 9 publications

(5 citation statements)

References 38 publications

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“…And this effect could be attenuated by MT receptor antagonist luzindole. It is corroborated by experimental result of Laurido et al [42] and Mauricio et al [40]. Wang et al [28] reported that melatonin improved mechanical hyperalgesia and depressive behaviors, down-regulated NR1 subunit of the NMDA receptor in rat TMJ inflammatory model.…”

Section: N-methyl-d-aspartate (Nmda) Receptorsupporting

confidence: 57%

“…NMDA receptor was another important factor involved in pain modulation of melatonin, especially in peripheral and central sensitization [20]. Evidences showed that spinal cord synaptic potentiation phenomenon called windup activity was significant in the development and maintenance of chronic pain and pain transmission which NMDA receptor plays an important role in spinal wind-up effect [40]- [42]. Noseda et al [41] reported that melatonin it induced dose dependent inhibition of wind-up activity.…”

Section: N-methyl-d-aspartate (Nmda) Receptormentioning

confidence: 99%

See 1 more Smart Citation

Melatonin in Pain Modulation: Analgesic or Proalgesic?

Liu¹,

He²,

Huang³

2014

PST

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Melatonin, as an endogenous hormone produced mainly in the pineal gland in a clear circadian fashion, has diverse physiological functions, such as the control of circadian rhythms, sleep regulation, antioxidant, etc. Recently, accumulating researches about melatonin and pain have been reported. In this review, comparison and summary about analgesic/proalgesic effect of melatonin in inflammatory and neuropathic pain will be made. Some possible pathways of melatonin involved in dual pain modulation might help to explain all these conflicting results in various situations.

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Section: N-methyl-d-aspartate (Nmda) Receptorsupporting

confidence: 57%

Section: N-methyl-d-aspartate (Nmda) Receptormentioning

confidence: 99%

Melatonin in Pain Modulation: Analgesic or Proalgesic?

Liu¹,

He²,

Huang³

2014

PST

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“…Their relevance in the central nervous system was recently reviewed [20]. In the spinal cord, an inhibitory effect of melatonin on nociceptive transmission was maintained by eserine [107]. In Xenopus melanophores, a loss of responsiveness to melatonin was prevented by the same drug [108].…”

Section: Tissue Versus Circulating Melatoninmentioning

confidence: 99%

Melatonin, hormone of darkness and more – occurrence, control mechanisms, actions and bioactive metabolites

Hardeland

2008

Cell. Mol. Life Sci.

222

202

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In its role as a pineal hormone, melatonin is a pleiotropic, nocturnally peaking and systemically acting chronobiotic. These effects are largely explained by actions via G protein-coupled membrane receptors found in the suprachiasmatic nucleus, but also in numerous other sites. Nuclear (ROR/RZR), cytoplasmic (quinone reductase-2, calmodulin, calreticulin) and mitochondrial binding sites and radical-scavenging properties contribute to the actions of melatonin. Regulation of pineal melatonin biosynthesis is largely explained by control mechanisms acting on arylalkylamine N-acetyltransferase, at the levels of gene expression and/or enzyme stability influenced by phosphorylation and interaction with 14-3-3 proteins. Melatonin is not only a hormone but is also synthesized in numerous extrapineal sites, in which it sometimes attains much higher quantities than in the pineal and the circulation. It is also present in many taxonomically distant groups of organisms, including bacteria, fungi, and plants. Moreover, melatonin is a source of bioactive metabolites, such as 5-methoxytryptamine, N(1)-acetyl-N(2)-formyl-5-methoxykynuramine and N(1)-acetyl-5-methoxykynuramine.

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“…Mondaca and colleagues34 recently studied the involvement of melatonin metabolites in the long‐term inhibitory effect of the hormone on rat spinal nociceptive transmission. This is based on the premise that melatonin and its metabolites could bind to nuclear sites in neurons, suggesting that this hormone is able to exert long‐term functional effects in the CNS via genomic mechanisms.…”

Section: Aβ Peptides Cholinesterase and Neurodegenerationmentioning

confidence: 99%

Amyloid, Cholinesterase, Melatonin, and Metals and Their Roles in Aging and Neurodegenerative Diseases

Lahiri

Chen

Lahiri

et al. 2005

Annals of the New York Academy of Sciences

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The aging brain shows selective neurochemical changes involving several neural cell populations. Increased brain metal levels have been associated with normal aging and a variety of diseases, including Alzheimer's disease (AD). Melatonin levels are decreased in aging, particularly in AD subjects. The loss of melatonin, which is synthesized by the pineal gland, together with the degeneration of cholinergic neurons of the basal forebrain and the deposition of aggregated proteins, such as the amyloid beta peptides (Abeta), are believed to contribute to the development of cognitive symptoms of dementia. Aging and its variants, such as AD, should be viewed as the result of multiple "hits," including alterations in the levels of Abeta, metals, cholinesterase enzymes, and neuronal gene expression. Herein, we present evidence in support of this theory, based on several studies. We discuss melatonin's neuroprotective function, which plays an important role in aging, prolongation of life span, and health in the aged individual. It interacts with metals and, in some cases, neutralizes their toxic effects. Dietary supplementation of melatonin restores its age-related loss. In mice, an elevated brain melatonin significantly reduced levels of potentially toxic Abeta peptides. Thus, compensation of melatonin loss in aging by dietary supplementation could well be beneficial in terms of reducing metal-induced toxicity, lipid peroxidation, and losses in cholinergic signaling. We propose that certain cholinesterase inhibitors and the NMDA partial antagonist memantine, which are FDA-approved drugs for AD and useful to boost central nervous system functioning, can be made more effective by their combination with melatonin or other neuroprotectants. Herein, we highlight studies elucidating the role of the amyloid pathway, metals, melatonin, and the cholinergic system in the context of aging and AD. Finally, melatonin is present in edible plants and walnuts, and consuming foodstuffs containing melatonin would be beneficial by enhancing the antioxidative capacity of the organisms.

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Involvement of melatonin metabolites in the long-term inhibitory effect of the hormone on rat spinal nociceptive transmission

Cited by 9 publications

References 38 publications

Melatonin in Pain Modulation: Analgesic or Proalgesic?

Melatonin in Pain Modulation: Analgesic or Proalgesic?

Melatonin, hormone of darkness and more – occurrence, control mechanisms, actions and bioactive metabolites

Amyloid, Cholinesterase, Melatonin, and Metals and Their Roles in Aging and Neurodegenerative Diseases

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