Melatonin enhances the rewarding properties of morphine: involvement of the nitric oxidergic pathway

Yahyavi-Firouz-Abadi, Noushin; Tahsili-Fahadan, Pouya; Ghahremani, Mohammad Hossein; Dehpour, Ahmad Reza

doi:10.1111/j.1600-079x.2007.00422.x

Cited by 13 publications

(6 citation statements)

References 56 publications

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“…1998; Chetsawang and Govitrapong 2005), but this increased melatonin level and disrupted circadian rhythm was not known to persist during 60 days of protracted withdrawal. Since melatonin can enhance the rewarding properties of morphine through nitric oxide pathways, its elevation may contribute to an enhanced priming effect of even a single morphine use leading to a full relapse to addiction (Yahyavi‐Firouz‐Abadi et al. 2007).…”

Section: Discussionmentioning

confidence: 99%

Circadian alteration in neurobiology during protracted opiate withdrawal in rats

Liu

Jiang

et al. 2010

Journal of Neurochemistry

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J. Neurochem. (2010) 115, 353–362. Abstract Protracted opiate withdrawal can extend for months of disrupted hormonal circadian rhythms. We examined rodent behaviors and these circadian disturbances in hormone and peptide levels as well as brain clock gene expression during 60 days of protracted withdrawal. Our behavioral tests included open field, elevated plus maze, and sucrose preference tests at 36 h, 10, 30, and 60 days after stopping chronic morphine. At these four assessment points, we collected samples every 4 h for 24 h to examine circadian rhythms in blood hormone and peptide levels and brain expression of rPER1, rPER2, and rPER3 clock genes. Decreased locomotor activity and elevated adrenocorticotropic hormone and melatonin levels persisted for 2 months after morphine withdrawal, but corticosterone was elevated only at 36 h and 10 days after withdrawal. Orexin levels were high at 36 h after withdrawal, but then reversed during protracted withdrawal to abnormally low levels. Beta‐endorphin (β‐EP) levels showed no differences from normal. However, circadian rhythms were blunted for all of these hormones. Corticosterone, adrenocorticotropic hormone, and orexin blunting persisted at least for 60 days. The blunted circadian rhythm of β‐EP and melatonin recovered by day 60, but the peak phase of β‐EP was delayed about 8 h. Blunted circadian rhythms and reduced expression of rPER1, rPER2, and rPER3 persisted at least for 60 days in the suprachiasmatic nucleus, prefrontal cortex, nucleus accumbens core, central nucleus of the amygdala, Hippocampus, and ventral tegmental area. Circadian rhythms of rPER1 in the nucleus accumbens shell and basolateral nucleus of the amygdala and of rPER2 in the central nucleus of the amygdala were reversed. Disrupted circadian rhythms of rPER1, rPER 2, and rPER3 expression in reward‐related brain circuits and blunted circadian rhythms in peripheral hormones and peptides may play a role in protracted opiate withdrawal and contribute to relapse.

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Section: Discussionmentioning

confidence: 99%

Circadian alteration in neurobiology during protracted opiate withdrawal in rats

Liu

Jiang

et al. 2010

Journal of Neurochemistry

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“…In an epilepsy model induced by pentylenetetrazole (PTZ), intraperitoneal melatonin administration (40 and 80 mg/kg) was found to significantly increase the seizure threshold of the animals through the NO/ l -arginine pathway . In further support, studies have also suggested that melatonin may enhance the antiseizure effects of morphine through the NO pathway. , …”

Section: Role Of Melatonin On the Pathological Pathways Of Epilepsymentioning

confidence: 95%

Melatonin as an Antiepileptic Molecule: Therapeutic Implications via Neuroprotective and Inflammatory Mechanisms

Akyüz

Küllü

Arulsamy

et al. 2021

ACS Chem. Neurosci.

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Epilepsy is a result of unprovoked, uncontrollable, and repetitive outburst of abnormal and excessive electrical discharges, known as seizures, in the neurons. Epilepsy is a devastating neurological condition that affects 70 million people globally. Unfortunately, only two-thirds of epilepsy patients respond to antiepileptic drugs while others become drug resistant and may be more prone to epilepsy comorbidities such as SUDEP. Oxidative stress, mitochondrial dysfunction, imbalance in the excitatory and inhibitory neurotransmitters, and neuroinflammation are some of the common pathologies of neurological disorders and epilepsy. Studies suggests that melatonin, a pineal hormone that governs sleep−wake cycles, may be neuroprotective against neurological disorders and thus may be translated as an antiepileptic as well. Melatonin has been shown to be an antioxidant, antiexcitotoxic, and anti-inflammatory hormone/ molecule in neurodegenerative diseases, which may contribute to its antiepileptic and neuroprotective properties in epilepsy as well. In addition, melatonin has evidently been shown to play a regulatory role in the cardiorespiratory system and sleep−wake cycles, which may have positive implications toward epilepsy associated comorbidities, such as SUDEP. However, studies investigating the changes in melatonin release due to epilepsy and melatonin's antiepileptic role have been inconclusive and scarce, respectively. Thus, this comprehensive review aims to summarize and elucidate the potential role of melatonin in the pathogenesis of epilepsy and its comorbidities, in hopes to develop new diagnostic and therapeutic approaches that will improve the lives of epileptic patients, particularly those who are drug resistant.

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“…was performed twice a day for 17 days from PND 35 to 51. The dosing regimen of melatonin was based on previous studies ( Yamamoto and Mohanan, 2003 ; Yahyavi-Firouz-Abade et al, 2007 ) and our pilot study ( Dang et al, 2014 ).…”

Section: Methodsmentioning

confidence: 99%

Melatonin Attenuates Memory Impairment Induced by Klotho Gene Deficiency Via Interactive Signaling Between MT2 Receptor, ERK, and Nrf2-Related Antioxidant Potential

Shin

Chung

et al. 2015

International Journal of Neuropsychopharmacology

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Background:We demonstrated that oxidative stress plays a crucial role in cognitive impairment in klotho mutant mice, a genetic model of aging. Since down-regulation of melatonin due to aging is well documented, we used this genetic model to determine whether the antioxidant property of melatonin affects memory impairment.Methods:First, we examined the effects of melatonin on hippocampal oxidative parameters and the glutathione/oxidized glutathione (GSH/GSSG) ratio and memory dysfunction of klotho mutant mice. Second, we investigated whether a specific melatonin receptor is involved in the melatonin-mediated pharmacological response by application with melatonin receptor antagonists. Third, we examined phospho-extracellular-signal-regulated kinase (ERK) expression, nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear translocation, Nrf2 DNA binding activity, and glutamate-cysteine ligase (GCL) mRNA expression. Finally, we examined effects of the ERK inhibitor SL327 in response to antioxidant efficacy and memory enhancement mediated by melatonin.Results:Treatment with melatonin resulted in significant attenuations of oxidative damage, a decrease in the GSH/GSSG ratio, and a significant amelioration of memory impairment in this aging model. These effects of melatonin were significantly counteracted by the selective MT2 receptor antagonist 4-P-PDOT. Importantly, 4-P-PDOT or SL327 also counteracted melatonin-mediated attenuation in response to the decreases in phospho-ERK expression, Nrf2 nuclear translocation, Nrf2 DNA-binding activity, and GCL mRNA expression in the hippocampi of klotho mutant mice. SL327 also counteracted the up-regulation of the GSH/GSSG ratio and the memory enhancement mediated by melatonin in klotho mutant mice.Conclusions:Melatonin attenuates oxidative stress and the associated memory impairment induced by klotho deficiency via signaling interaction between the MT2 receptor and ERK- and Nrf2-related antioxidant potential.

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Melatonin enhances the rewarding properties of morphine: involvement of the nitric oxidergic pathway

Cited by 13 publications

References 56 publications

Circadian alteration in neurobiology during protracted opiate withdrawal in rats

Circadian alteration in neurobiology during protracted opiate withdrawal in rats

Melatonin as an Antiepileptic Molecule: Therapeutic Implications via Neuroprotective and Inflammatory Mechanisms

Melatonin Attenuates Memory Impairment Induced by Klotho Gene Deficiency Via Interactive Signaling Between MT2 Receptor, ERK, and Nrf2-Related Antioxidant Potential

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