Journal articles: 'Melatonin. Nervous system'

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Hardeland, Rudiger. "Melatonin Metabolism in the Central Nervous System." Current Neuropharmacology 8, no. 3 (September 1, 2010): 168–81. http://dx.doi.org/10.2174/157015910792246164.

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Esposito, Emanuela, and Salvatore Cuzzocrea. "Antiinflammatory Activity of Melatonin in Central Nervous System." Current Neuropharmacology 8, no. 3 (September 1, 2010): 228–42. http://dx.doi.org/10.2174/157015910792246155.

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Stankov, Bojidar, Franco Fraschini, and Russel J. Reiter. "Melatonin binding sites in the central nervous system." Brain Research Reviews 16, no. 3 (September 1991): 245–56. http://dx.doi.org/10.1016/0165-0173(91)90008-v.

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Voiculescu, S. E., A. Rosca, C. M. D. Zahiu, C. Badiu, and A. M. Zagrean. "MELATONIN AND MONOAMINERGIC SYSTEM – BEHAVIOURAL ASPECTS." Romanian Journal of Neurology 15, no. 1 (March 31, 2016): 5–15. http://dx.doi.org/10.37897/rjn.2016.1.1.

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Melatonin, the hormone synthesized mainly by the pineal gland, is a key member of the complex monoaminergic signaling system, and a circadian regulator with pleiotropic functions. This ubiquitary lipophilic and hydrophilic molecule acts both at cellular and subcellular level, exerting anti-inflammatory, anti-oxidative and anti-apoptotic activities, extremely important in the nervous system, given its high vulnerability to oxidative injury. Melatonin deprivation and the consecutive chronodisruption are associated with multiple behavioural abnormalities, psychiatric disorders and neurodegenerative diseases. The present review summarizes the available information concerning the link between melatonin, monoaminergic neurotransmission and the pathophysiological bases of these conditions.

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Cardinali, Daniel P., Eleonora S. Pagano, Pablo A. Scacchi Bernasconi, Roxana Reynoso, and Pablo Scacchi. "Melatonin and mitochondrial dysfunction in the central nervous system." Hormones and Behavior 63, no. 2 (February 2013): 322–30. http://dx.doi.org/10.1016/j.yhbeh.2012.02.020.

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Mahle, Cathy D., and A. John Watson. "Melatonin receptors: potential targets for central nervous system disorders." Expert Opinion on Investigational Drugs 6, no. 4 (April 1997): 399–406. http://dx.doi.org/10.1517/13543784.6.4.399.

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Lu, Jianan, Yujie Luo, Shuhao Mei, Yuanjian Fang, Jianmin Zhang, and Sheng Chen. "The Effect of Melatonin Modulation of Non-coding RNAs on Central Nervous System Disorders: An Updated Review." Current Neuropharmacology 19, no. 1 (December 31, 2020): 3–23. http://dx.doi.org/10.2174/1570159x18666200503024700.

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: Melatonin is a hormone produced in and secreted by the pineal gland. Besides its role in regulating circadian rhythms, melatonin has a wide range of protective functions in the central nervous system (CNS) disorders. The mechanisms underlying this protective function are associated with the regulatory effects of melatonin on related genes and proteins. In addition to messenger ribonucleic acid (RNA) that can be translated into protein, an increasing number of non-coding RNAs in the human body are proven to participate in many diseases. This review discusses the current progress of research on the effects of melatonin modulation of non-coding RNAs (ncRNAs), including microRNA, long ncRNA, and circular RNA. The role of melatonin in regulating common pathological mechanisms through these ncRNAs is also summarized. Furthermore, the ncRNAs, currently shown to be involved in melatonin signaling in CNS diseases, are discussed. The information compiled in this review will open new avenues for future research into melatonin mechanisms and provide a further understanding of ncRNAs in the CNS.

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Ruddick, Jon P., Andrew K. Evans, David J. Nutt, Stafford L. Lightman, Graham A. W. Rook, and Christopher A. Lowry. "Tryptophan metabolism in the central nervous system: medical implications." Expert Reviews in Molecular Medicine 8, no. 20 (August 2006): 1–27. http://dx.doi.org/10.1017/s1462399406000068.

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The metabolism of the amino acid l-tryptophan is a highly regulated physiological process leading to the generation of several neuroactive compounds within the central nervous system. These include the aminergic neurotransmitter serotonin (5-hydroxytryptamine, 5-HT), products of the kynurenine pathway of tryptophan metabolism (including 3-hydroxykynurenine, 3-hydroxyanthranilic acid, quinolinic acid and kynurenic acid), the neurohormone melatonin, several neuroactive kynuramine metabolites of melatonin, and the trace amine tryptamine. The integral role of central serotonergic systems in the modulation of physiology and behaviour has been well documented since the first description of serotonergic neurons in the brain some 40 years ago. However, while the significance of the peripheral kynurenine pathway of tryptophan metabolism has also been recognised for several decades, it has only recently been appreciated that the synthesis of kynurenines within the central nervous system has important consequences for physiology and behaviour. Altered kynurenine metabolism has been implicated in the pathophysiology of conditions such as acquired immunodeficiency syndrome (AIDS)-related dementia, Huntington's disease and Alzheimer's disease. In this review we discuss the molecular mechanisms involved in regulating the metabolism of tryptophan and consider the medical implications associated with dysregulation of both serotonergic and kynurenine pathways of tryptophan metabolism.

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Sadanandan, Nadia, Blaise Cozene, Justin Cho, You Jeong Park, Madeline Saft, Bella Gonzales-Portillo, and Cesar V. Borlongan. "Melatonin—A Potent Therapeutic for Stroke and Stroke-Related Dementia." Antioxidants 9, no. 8 (July 28, 2020): 672. http://dx.doi.org/10.3390/antiox9080672.

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Secreted by the pineal gland to regulate the circadian rhythm, melatonin is a powerful antioxidant that has been used to combat oxidative stress in the central nervous system. Melatonin-based therapies have been shown to provide neuroprotective effects in the setting of ischemic stroke by mitigating neuroinflammation and accelerating brain tissue restoration. Melatonin treatment includes injection of exogenous melatonin, pineal gland grafting and melatonin-mediated stem cell therapy. This review will discuss the current preclinical and clinical studies investigating melatonin-based therapeutics to treat stroke.

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Reiter, Russel J. "Oxidative damage in the central nervous system: protection by melatonin." Progress in Neurobiology 56, no. 3 (October 1998): 359–84. http://dx.doi.org/10.1016/s0301-0082(98)00052-5.

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Samantaray, Supriti, Arabinda Das, Nakul P. Thakore, Denise D. Matzelle, Russel J. Reiter, Swapan K. Ray, and Naren L. Banik. "Therapeutic potential of melatonin in traumatic central nervous system injury." Journal of Pineal Research 47, no. 2 (September 2009): 134–42. http://dx.doi.org/10.1111/j.1600-079x.2009.00703.x.

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Sarlak, Golmaryam, Anorut Jenwitheesuk, Banthit Chetsawang, and Piyarat Govitrapong. "Effects of Melatonin on Nervous System Aging: Neurogenesis and Neurodegeneration." Journal of Pharmacological Sciences 123, no. 1 (2013): 9–24. http://dx.doi.org/10.1254/jphs.13r01sr.

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Kennaway, David J., and Helmut M. Hugel. "Mechanisms of action of melatonin within the central nervous system." Animal Reproduction Science 30, no. 1-3 (November 1992): 45–65. http://dx.doi.org/10.1016/0378-4320(92)90005-x.

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Juszczak, Kajetan, Agata Ziomber, Anna Machowska, Agata Furgała, Łukasz Dobrek, Marek Wyczółkowski, and Piotr J. Thor. "The Ameliorating Effect of Exogenous Melatonin on Urinary Bladder Function in Hyperosmolar Bladder Overactivity and its Influence on the Autonomic Nervous System Activity." Acta Medica (Hradec Kralove, Czech Republic) 54, no. 2 (2011): 63–68. http://dx.doi.org/10.14712/18059694.2016.20.

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This study was designed to investigate the effects of melatonin on the bladder hyperactivity in hyperosmolar-induced overactive bladder (OAB) rats. Additionally, the influence of melatonin on the autonomic nervous system (ANS) using heart rate variability (HRV) analysis was assessed. 40 rats were divided into four groups: I – control (n=12), II – rats with hyperosmolar OAB (n=6), III – rats with melatonin pretreatment and hyperosmolar OAB (n=6) and IV – control with melatonin pretreatment (n=6). In group III and IV melatonin in dose of 100 mg/kg was given. HRV measurements in 10 rats, as follow: control (n=2), control after melatonin treatment (n=2), rats with hyperosmolar OAB without (n=3), and after (n=3) melatonin treatment were conducted. This study demonstrates marked influence of melatonin on urinary bladder activity in hyperosmolar-induced OAB rats. These rats showed significantly reduced the detrusor motor overactivity resulting in the improvement of cystometric parameters after melatonin treatment when compared to the control, as follow: a significant increase of intercontraction interval (70 %) and functional bladder capacity (67 %), as well as a decrease of the basal pressure, detrusor overactivity index and motility index of 96 %, 439 % and 40 %, respectively. ANS activity analysis revealed sympathetic overactivity in OAB rats, and parasympathetic superiority in melatonin treated OAB rats. Melatonin treatment in rats with hyperosmolar OAB (group III) caused significant increase of nuHF parameter (from 51.00 ± 25.29 to 76.97 ± 17.43), as well as a decrease of nuLF parameter (from 49.01 ± 25.26 to 23.03 ± 17.43) and LF/HF ratio (from 1.280 ± 0.980 to 0.350 ± 0.330). In conclusion, melatonin suppresses hyperosmolar OAB, and modulates ANS activity by inhibition of the sympathetic drive. Therefore, melatonin may become a useful agent for OAB management.

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Kurtulmuş, Seda, and Tuğba Kök Taş. "Gıdalarda Bulunan L-Triptofan, Serotonin, Melatonin Profilleri ve Sağlık Üzerine Etkileri." Turkish Journal of Agriculture - Food Science and Technology 3, no. 11 (November 6, 2015): 877. http://dx.doi.org/10.24925/turjaf.v3i11.877-885.355.

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Nowadays, depending on the progress of science and technology, our eating habits have changed. The shape and quality of nutrition is important for human health. Especially, some food components have various effect on central nervous system such as depression, anxiety, sleep, appetite. Food constituents are transported into the central nervous system via the neutral amino acids such as phenylalanine, leucine, isoleucine, tyrosine and valine. Amino acids have an important role in human nutrition. It cannot be synthesized in the body and one of the essential amino acids that must be taken outside, trytophan, is indispensable in human nutrition because of it has the many functions. In recent years, scientific community concentrated on the various functions of L-Trytophan (L-Trp) as pioneer in the secretion of the hormones serotonin and melatoninin in the human body. The hormones serotonin and melatonin is responsible for activities such as psychology, sleep, body temperature, blood pressure balance, antioxidant effect, cancer inhibitor, sexuality, autism and circadian rhythms in human body that they are available in various foods such as milk, kefir, yogurt, orange, strawberry, grape, olive oil, walnut, prune, nut, pomegranate, coffee, kiwi and banana. In this study, L-Trp, serotonin and melatonin biosynthesis and metabolism, food profiles and in terms of their physiological and biological effects on human health has been compiled.

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Khalili, Zaynab, Parastoo Barati Dowom, Marzieh Darvishi, and Khadijeh Abdal. "An Overview of the Effects of Melatonin on Nervous System Diseases." Neuroscience Journal of Shefaye Khatam 7, no. 3 (July 1, 2019): 61–73. http://dx.doi.org/10.29252/shefa.7.3.61.

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H. Limon-Pacheco, Jorge, and Maria E. Gonsebatt. "The Glutathione System and its Regulation by Neurohormone Melatonin in the Central Nervous System." Central Nervous System Agents in Medicinal Chemistry 10, no. 4 (December 1, 2010): 287–97. http://dx.doi.org/10.2174/187152410793429683.

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López-Valverde, Nansi, Beatriz Pardal-Peláez, Antonio López-Valverde, and Juan Manuel Ramírez. "Role of Melatonin in Bone Remodeling around Titanium Dental Implants: Meta-Analysis." Coatings 11, no. 3 (February 25, 2021): 271. http://dx.doi.org/10.3390/coatings11030271.

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The theory, known as the “brain-bone axis” theory, involves the central nervous system in bone remodeling. The alteration of the nervous system could lead to abnormal bone remodeling. Melatonin produced by the pineal gland is a hormone that is characterized by its antioxidant properties. The aim of this meta-analysis was to examine the role of melatonin in the growth of new bone around titanium dental implants in vivo. A manual search of the PubMed and Web of Science databases was conducted to identify scientific studies published until November 2020. We included randomized clinical trials (RCTs) and animal studies where melatonin was used with titanium implants. Fourteen studies met the inclusion criteria. Quality was assessed using the Jadad scale and SYRCLE’s risk of bias tool. Our meta-analysis revealed that the use of melatonin during implant placement improves bone-to-implant contact percentages in animals (difference of means, random effects: 9.59 [95% CI: 5.53–13.65]), reducing crestal bone loss in humans (difference in means, random effects: −0.55 [95% CI: 1.10–0.00]). In animals, titanium implants using melatonin increase bone-to-implant contact surface 2–6 weeks after their placement and reduce crestal bone loss in humans following six months. The results of this meta-analysis should be taken with caution, due to the small samples and the large heterogeneity among studies.

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Song, Juhyun, So Mang Kang, Won Taek Lee, Kyung Ah Park, Kyoung Min Lee, and Jong Eun Lee. "The Beneficial Effect of Melatonin in Brain Endothelial Cells against Oxygen-Glucose Deprivation Followed by Reperfusion-Induced Injury." Oxidative Medicine and Cellular Longevity 2014 (2014): 1–14. http://dx.doi.org/10.1155/2014/639531.

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Melatonin has a cellular protective effect in cerebrovascular and neurodegenerative diseases. Protection of brain endothelial cells against hypoxia and oxidative stress is important for treatment of central nervous system (CNS) diseases, since brain endothelial cells constitute the blood brain barrier (BBB). In the present study, we investigated the protective effect of melatonin against oxygen-glucose deprivation, followed by reperfusion- (OGD/R-) induced injury, in bEnd.3 cells. The effect of melatonin was examined by western blot analysis, cell viability assays, measurement of intracellular reactive oxygen species (ROS), and immunocytochemistry (ICC). Our results showed that treatment with melatonin prevents cell death and degradation of tight junction protein in the setting of OGD/R-induced injury. In response to OGD/R injury of bEnd.3 cells, melatonin activates Akt, which promotes cell survival, and attenuates phosphorylation of JNK, which triggers apoptosis. Thus, melatonin protects bEnd.3 cells against OGD/R-induced injury.

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Yamanaka, Yujiro, Satoko Hashimoto, Nana N. Takasu, Yusuke Tanahashi, Shin-ya Nishide, Sato Honma, and Ken-ichi Honma. "Morning and evening physical exercise differentially regulate the autonomic nervous system during nocturnal sleep in humans." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 309, no. 9 (November 1, 2015): R1112—R1121. http://dx.doi.org/10.1152/ajpregu.00127.2015.

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Effects of daily physical exercise in the morning or in the evening were examined on circadian rhythms in plasma melatonin and core body temperature of healthy young males who stayed in an experimental facility for 7 days under dim light conditions (<10 lux). Sleep polysomnogram (PSG) and heart rate variability (HRV) were also measured. Subjects performed 2-h intermittent physical exercise with a bicycle ergometer at ZT3 or at ZT10 for four consecutive days, where zeitgeber time 0 (ZT0) was the time of wake-up. The rising phase of plasma melatonin rhythm was delayed by 1.1 h without exercise. Phase-delay shifts of a similar extent were detected by morning and evening exercise. But the falling phase shifted only after evening exercise by 1.0 h. The sleep PSG did not change after morning exercise, while Stage 1+2 sleep significantly decreased by 13.0% without exercise, and RE sleep decreased by 10.5% after evening exercise. The nocturnal decline of rectal temperature was attenuated by evening exercise, but not by morning exercise. HRV during sleep changed differentially. Very low frequency (VLF) waves increased without exercise. VLF, low frequency (LF), and high frequency (HF) waves increased after morning exercise, whereas HR increased after evening exercise. Morning exercise eventually enhanced the parasympathetic activity, as indicated by HRV, while evening exercise activated the sympathetic activity, as indicated by increase in heart rate in the following nocturnal sleep. These findings indicated differential effects of morning and evening exercise on the circadian melatonin rhythm, PSG, and HRV.

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Campos, Luciana A., Jose Cipolla-Neto, Fernanda G. Amaral, Lisete C. Michelini, Michael Bader, and Ovidiu C. Baltatu. "The Angiotensin-Melatonin Axis." International Journal of Hypertension 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/521783.

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Accumulating evidence indicates that various biological and neuroendocrine circadian rhythms may be disrupted in cardiovascular and metabolic disorders. These circadian alterations may contribute to the progression of disease. Our studies direct to an important role of angiotensin II and melatonin in the modulation of circadian rhythms. The brain renin-angiotensin system (RAS) may modulate melatonin synthesis, a hormone with well-established roles in regulating circadian rhythms. Angiotensin production in the central nervous system may not only influence hypertension but also appears to affect the circadian rhythm of blood pressure. Drugs acting on RAS have been proven effective in the treatment of cardiovascular and metabolic disorders including hypertension and diabetes mellitus (DM). On the other hand, since melatonin is capable of ameliorating metabolic abnormalities in DM and insulin resistance, the beneficial effects of RAS blockade could be improved through combined RAS blocker and melatonin therapy. Contemporary research is evidencing the existence of specific clock genes forming central and peripheral clocks governing circadian rhythms. Further research on the interaction between these two neurohormones and the clock genes governing circadian clocks may progress our understanding on the pathophysiology of disease with possible impact on chronotherapeutic strategies.

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Labunets, I. F., N. A. Utko, T. N. Panteleymonova, and G. M. Butenko. "The effect of exogenous melatonin on behavior and oxidative stress indicators in the brain of aging mice with experimental models of nervous system pathology." INTERNATIONAL NEUROLOGICAL JOURNAL 17, no. 2 (May 19, 2021): 37–43. http://dx.doi.org/10.22141/2224-0713.17.2.2021.229893.

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Background. There is a connection between impaired functioning of the nervous system and oxidative stress in Parkinson’s disease and multiple sclerosis. The influence of age on the development of these pathologies was shown, as well as the antioxidant properties of the hormone melatonin. The purpose was to investigate the effect of melatonin administration on the behavior, factors of oxidative stress and antioxidant protection in the brain of aging mice with experimental models of parkinsonism and demyelination. Materials and methods. 129/Sv mice aged 15–16 months received neurotoxins 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) at a dose of 30 mg/kg once, or cuprizone daily with food for 3 weeks. Melatonin was administered at a dose of 1 mg/kg daily at 6 p.m. starting from day 7–8 of toxin exposure. The content of malondialdehyde, the activity of antioxidant enzymes in the brain and behavior parameters were assessed in the open field tests for rigidity and in the rotarod test. Results. The locomotor, emotional and exploratory activities in mice with parkinsonism and demyelination models are lower than those in intact animals. Muscle tone decreases under the influence of cuprizone and increases after MPTP injection; the step length decreases in parkinsonism. Melatonin treatment resulted in increasing the number of squares, step length, and decreasing the retention time on a rotating cylinder in mice with parkinsonism and increasing the number of squares, rea-ring and number of boluses in cuprizone-treated mice. Exogenous melatonin reduces the level of brain malondialdehyde increased by neurotoxins and increases the reduced activity of superoxide dismutase and catalase in mice with parkinsonism, catalase and glutathione peroxidase in mice with demyelination. Conclusions. The positive effects of melatonin on the behavior of aging mice with the MPTP parkinsonism model and the cuprizone model of demyeli-nation are mediated by increased antioxidant protection in the brain.

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Gurunathan, Sangiliyandi, Min-Hee Kang, and Jin-Hoi Kim. "Role and Therapeutic Potential of Melatonin in the Central Nervous System and Cancers." Cancers 12, no. 6 (June 13, 2020): 1567. http://dx.doi.org/10.3390/cancers12061567.

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Melatonin (MLT) is a powerful chronobiotic hormone that controls a multitude of circadian rhythms at several levels and, in recent times, has garnered considerable attention both from academia and industry. In several studies, MLT has been discussed as a potent neuroprotectant, anti-apoptotic, anti-inflammatory, and antioxidative agent with no serious undesired side effects. These characteristics raise hopes that it could be used in humans for central nervous system (CNS)-related disorders. MLT is mainly secreted in the mammalian pineal gland during the dark phase, and it is associated with circadian rhythms. However, the production of MLT is not only restricted to the pineal gland; it also occurs in the retina, Harderian glands, gut, ovary, testes, bone marrow, and lens. Although most studies are limited to investigating the role of MLT in the CNS and related disorders, we explored a considerable amount of the existing literature. The objectives of this comprehensive review were to evaluate the impact of MLT on the CNS from the published literature, specifically to address the biological functions and potential mechanism of action of MLT in the CNS. We document the effectiveness of MLT in various animal models of brain injury and its curative effects in humans. Furthermore, this review discusses the synthesis, biology, function, and role of MLT in brain damage, and as a neuroprotective, antioxidative, anti-inflammatory, and anticancer agent through a collection of experimental evidence. Finally, it focuses on the effect of MLT on several neurological diseases, particularly CNS-related injuries.

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KOPPITZ, P., M. STORR, D. SAUR, M. KURJAK, and H. ALLESCHER. "Inhibitory effect of melatonin on nitric oxide synthase in rat enteric nervous system." Gastroenterology 120, no. 5 (April 2001): A176. http://dx.doi.org/10.1016/s0016-5085(01)80869-6.

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Hardeland, R., and B. Poeggeler. "Melatonin and Synthetic Melatonergic Agonists: Actions and Metabolism in the Central Nervous System." Central Nervous System Agents in Medicinal Chemistry 12, no. 3 (August 1, 2012): 189–216. http://dx.doi.org/10.2174/187152412802430129.

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Koppitz, Patrick B., Martin A. Storr, Dieter Saur, Manfred Kurjak, and Hans-Dieter Allescher. "Inhibitory effect of melatonin on nitric oxide synthase in rat enteric nervous system." Gastroenterology 120, no. 5 (April 2001): A176. http://dx.doi.org/10.1016/s0016-5085(08)80869-4.

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Faria, Juliana A., Andrezza Kinote, Letícia M. Ignacio-Souza, Thiago M. de Araújo, Daniela S. Razolli, Diego L. Doneda, Lívia B. Paschoal, et al. "Melatonin acts through MT1/MT2 receptors to activate hypothalamic Akt and suppress hepatic gluconeogenesis in rats." American Journal of Physiology-Endocrinology and Metabolism 305, no. 2 (July 15, 2013): E230—E242. http://dx.doi.org/10.1152/ajpendo.00094.2013.

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Melatonin can contribute to glucose homeostasis either by decreasing gluconeogenesis or by counteracting insulin resistance in distinct models of obesity. However, the precise mechanism through which melatonin controls glucose homeostasis is not completely understood. Male Wistar rats were administered an intracerebroventricular (icv) injection of melatonin and one of following: an icv injection of a phosphatidylinositol 3-kinase (PI3K) inhibitor, an icv injection of a melatonin receptor (MT) antagonist, or an intraperitoneal (ip) injection of a muscarinic receptor antagonist. Anesthetized rats were subjected to pyruvate tolerance test to estimate in vivo glucose clearance after pyruvate load and in situ liver perfusion to assess hepatic gluconeogenesis. The hypothalamus was removed to determine Akt phosphorylation. Melatonin injections in the central nervous system suppressed hepatic gluconeogenesis and increased hypothalamic Akt phosphorylation. These effects of melatonin were suppressed either by icv injections of PI3K inhibitors and MT antagonists and by ip injection of a muscarinic receptor antagonist. We conclude that melatonin activates hypothalamus-liver communication that may contribute to circadian adjustments of gluconeogenesis. These data further suggest a physiopathological relationship between the circadian disruptions in metabolism and reduced levels of melatonin found in type 2 diabetes patients.

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Chen, Dongmei, Tao Zhang, and Tae Ho Lee. "Cellular Mechanisms of Melatonin: Insight from Neurodegenerative Diseases." Biomolecules 10, no. 8 (August 7, 2020): 1158. http://dx.doi.org/10.3390/biom10081158.

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Neurodegenerative diseases are the second most common cause of death and characterized by progressive impairments in movement or mental functioning in the central or peripheral nervous system. The prevention of neurodegenerative disorders has become an emerging public health challenge for our society. Melatonin, a pineal hormone, has various physiological functions in the brain, including regulating circadian rhythms, clearing free radicals, inhibiting biomolecular oxidation, and suppressing neuroinflammation. Cumulative evidence indicates that melatonin has a wide range of neuroprotective roles by regulating pathophysiological mechanisms and signaling pathways. Moreover, melatonin levels are decreased in patients with neurodegenerative diseases. In this review, we summarize current knowledge on the regulation, molecular mechanisms and biological functions of melatonin in neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, vascular dementia and multiple sclerosis. We also discuss the clinical application of melatonin in neurodegenerative disorders. This information will lead to a better understanding of the regulation of melatonin in the brain and provide therapeutic options for the treatment of various neurodegenerative diseases.

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Kalmukova, O., and M. Dzerzhynsky. "Morpho-functional state of rats pineal gland and suprachismatic nucleus of hypothalamus after different regimes of exogenous melatonin administration." Bulletin of Taras Shevchenko National University of Kyiv. Series: Biology 83, no. 4 (2020): 17–23. http://dx.doi.org/10.17721/1728_2748.2020.83.17-23.

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In modern society increase of digitalization associated with grown exceed level of light at night – a new type of pollution. Presence of light at night inhibited endogenous melatonin synthesis by pineal gland, that influence on circadian system work cycles, so organism oftenbroken regime of wake/sleep, meals, physical activity. Also, a lack of melatonin in some certain time of dayand low melatonin concentration both, were shown take some intervention in diseases development through incorrect regulation of clock-depended genes expression. In connect with this, some latest clinical protocol in therapy or clinical trials of many different pathologies (for example, insomnia, metabolic syndrome, cardiovascular diseases, central nervous and immune system trouble, cancer, viral infection, etc.) include exogenous melatonin usage. As melatonin perform his function via endocrine and paracrine ways in variety types of cell, his application take place in wide range of doses and in different time of day (chronotherapeutic approach). Therefore, important to control state of circadian system central elements – pineal gland (main producer of endogenous melatonin) and suprachiasmatic nucleus (SCN) of hypothalamus (central pacemaker of circadian rhythm) in conditionsof exogenous melatonin treatment. Thus, the main goal of our research were analysis of rats pineal gland and hypothalamic SCN morpho-functional state after different time (morning, evening and continuously with drinking water) melatonin daily administration. Melatonin was administered by gavage for 7 weeks in dose 30 mg/kg 1 h before lights-off (M ZT11, evening), or 1 h after lights-on (M ZT01, morning), or continuously with drinking water during day-night period (MW). After melatonin use only in MW group pineal gland demonstrates changes in morphology (pinealocytes nucleus had mild basophilic color) and morphometric (increased cross-sectional area of the pinealocytes nucleus in compare with control group) analysis data. Besides, some similar changes were observed in SCN: the cross-sectional area of the SCN neurons nucleus grown in case of usage each of regime melatonin administration, while morphology characteristic remains without any alteration. In general, it suggesting about having by melatonin non-inhibiting features in context of circadian system feedback loop and supposing wide potential for melatonin use with absent huge side effect on central elements of above mentioned system.

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Uyanikgil, Yigit, Turker Cavusoglu, Kubilay Kılıc, Gurkan Yigitturk, Servet Celik, Richard Tubbs, and Mehmet Turgut. "Useful Effects of Melatonin in Peripheral Nerve Injury and Development of the Nervous System." Journal of Brachial Plexus and Peripheral Nerve Injury 12, no. 01 (January 2017): e1-e6. http://dx.doi.org/10.1055/s-0036-1597838.

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This review summarizes the role of melatonin (MLT) in defense against toxic-free radicals and its novel effects in the development of the nervous system, and the effect of endogenously produced and exogenously administered MLT in reducing the degree of tissue and nerve injuries. MLT was recently reported to be an effective free radical scavenger and antioxidant. Since endogenous MLT levels fall significantly in senility, these findings imply that the loss of this antioxidant could contribute to the incidence or severity of some age-related neurodegenerative diseases. Considering the high efficacy of MLT in overcoming much of the injury not only to the peripheral nerve but also to other organs, clinical trials for this purpose should be seriously considered.

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Tsenteradze, S. L., and M. G. Poluektov. "Therapeutic aspects of melatonin applications." Meditsinskiy sovet = Medical Council, no. 10 (August 12, 2021): 80–84. http://dx.doi.org/10.21518/2079-701x-2021-10-80-84.

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The results of multicenter clinical trials show the broad potential of melatonin since discovery of this adaptogen to the present day. Melatonin is a neuropeptide that is synthesized mainly in the small brain gland, the pineal gland, and has a unique effect in humans and animals. Using melatonin, the pineal gland participates in the organization of circadian periodism and regulation of cyclic processes, acting as an intermediary between the pacemaker mechanism of the suprachiasmatic nuclei (SCN) and peripheral organs. The pineal gland and the SCN of the hypothalamus form part of the system of the so-called biological clock of the body, which plays a key role in the mechanisms of regulation of the biological clock via circadian rhythms and ageing. Initially, melatonin was only considered a hormone involved in the synchronization of the mechanisms of the circadian rhythm, but later it was found that, in addition to this hormonal function, it takes part in the regulation of the seasonal cycle in animals and humans.At present, melatonin drugs have shown high efficacy and safety in various sleep-wake disorders regardless of their genesis, disorganization of circadian rhythms, stress adjustment disorders, rapid change of time zones, shift work and in complex therapy of patients with cerebrovascular diseases.The article considers the multimodal capabilities of melatonin, including adaptogenic, biorhythmogenic, hypnotic, immunostimu-lating, antioxidant effects. The role of melatonin in the treatment of various central nervous system disorders, including neurodegenerative diseases, has been determined.The review emphasizes the wide-ranging effects of melatonin and offers great opportunities for measuring melatonin as a biomarker for early detection and follow-up of various diseases.

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Herman, A. P., J. Bochenek, K. Król, A. Krawczyńska, H. Antushevich, B. Pawlina, A. Herman, K. Romanowicz, and D. Tomaszewska-Zaremba. "Central Interleukin-1βSuppresses the Nocturnal Secretion of Melatonin." Mediators of Inflammation 2016 (2016): 1–15. http://dx.doi.org/10.1155/2016/2589483.

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In vertebrates, numerous processes occur in a rhythmic manner. The hormonal signal reliably reflecting the environmental light conditions is melatonin. Nocturnal melatonin secretion patterns could be disturbed in pathophysiological states, including inflammation, Alzheimer’s disease, and depression. All of these states share common elements in their aetiology, including the overexpression of interleukin- (IL-) 1βin the central nervous system. Therefore, the present study was designed to determine the effect of the central injection of exogenous IL-1βon melatonin release and on the expression of the enzymes of the melatonin biosynthetic pathway in the pineal gland of ewe. It was found that intracerebroventricular injections of IL-1β(50 µg/animal) suppressed(P<0.05)nocturnal melatonin secretion in sheep regardless of the photoperiod. This may have resulted from decreased(P<0.05)synthesis of the melatonin intermediate serotonin, which may have resulted, at least partially, from a reduced expression of tryptophan hydroxylase. IL-1βalso inhibited(P<0.05)the expression of the melatonin rhythm enzyme arylalkylamine-N-acetyltransferase and hydroxyindole-O-methyltransferase. However, the ability of IL-1βto affect the expression of these enzymes was dependent upon the photoperiod. Our study may shed new light on the role of central IL-1βin the aetiology of disruptions in melatonin secretion.

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Liu, Mu-Tai, and Russel J. Reiter. "Molecular mechanisms of melatonin’s protection against high-LET radiation: implications for space travel." Melatonin Research 3, no. 4 (October 9, 2020): 503–14. http://dx.doi.org/10.32794/mr11250075.

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During a deep space mission, the central nervous system (CNS) and other organs are exposed to galactic cosmic rays and solar particle events. Health risks associated with various organs and systems are important issues in a long-term spaceflight. Potential CNS damage during a space mission could alter cognitive functions which might impact performance and individual’s health. The neuronal injury originating from exposure to 56Fe particle irradiation involves the elevated oxidative stress which can be inhibited by melatonin pretreatment. Melatonin exerts potent neuroprotective effects against carbon ion-induced mitochondrial dysfunction and apoptosis in the mouse brain. A significant increase in the count of immature neurons and proliferating cells was detected in the mice under 56Fe particle irradiation cotreated with the melatonin metabolite, AFMK. Melatonin treatment also significantly reduced the carbon ion-induced apoptotic cells and elevated oxidative stress in the mouse testis. The results suggest that melatonin treatment is a potential strategy to protect against space radiation hazards. Spaceflight-induced molecular, cellular, and physiologic changes lead to alterations across many organs and systems. Epigenetic, gene expression, inflammatory, and metabolic responses to spaceflight should be examined and means to safe-guard against these changes in upcoming missions. Precision medicine will be crucial for assessing and augmenting efficacy of melatonin or other medications in astronauts. In addition, enhancing radio-resistance of humans is a novel strategy for a long-term space mission. Further investigations with a combination of melatonin and other novel technologies are warranted to better alleviate HZE particle irradiation-induced damage to astronauts on long-term space exploration missions.

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Leung, Joseph Wai-Hin, Kwok-Kuen Cheung, Shirley Pui-Ching Ngai, Hector Wing-Hong Tsang, and Benson Wui-Man Lau. "Protective Effects of Melatonin on Neurogenesis Impairment in Neurological Disorders and Its Relevant Molecular Mechanisms." International Journal of Molecular Sciences 21, no. 16 (August 6, 2020): 5645. http://dx.doi.org/10.3390/ijms21165645.

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Neurogenesis is the process by which functional new neurons are generated from the neural stem cells (NSCs) or neural progenitor cells (NPCs). Increasing lines of evidence show that neurogenesis impairment is involved in different neurological illnesses, including mood disorders, neurogenerative diseases, and central nervous system (CNS) injuries. Since reversing neurogenesis impairment was found to improve neurological outcomes in the pathological conditions, it is speculated that modulating neurogenesis is a potential therapeutic strategy for neurological diseases. Among different modulators of neurogenesis, melatonin is a particularly interesting one. In traditional understanding, melatonin controls the circadian rhythm and sleep–wake cycle, although it is not directly involved in the proliferation and survival of neurons. In the last decade, it was reported that melatonin plays an important role in the regulation of neurogenesis, and thus it may be a potential treatment for neurogenesis-related disorders. The present review aims to summarize and discuss the recent findings regarding the protective effects of melatonin on the neurogenesis impairment in different neurological conditions. We also address the molecular mechanisms involved in the actions of melatonin in neurogenesis modulation.

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Babaee, Abdolreza, Seyed Hassan Eftekhar Vaghefi, Samereh Dehghani Soltani, Majid Asadi Shekaari, Nader Shahrokhi, and Mohsen Basiri. "Hippocampal Astrocyte Response to Melatonin Following Neural Damage Induction in Rats." Basic and Clinical Neuroscience Journal 12, no. 2 (March 1, 2021): 177–86. http://dx.doi.org/10.32598/bcn.12.2.986.1.

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Introduction: Brain injury induces an almost immediate response from glial cells, especially astrocytes. Activation of astrocytes leads to the production of inflammatory cytokines and reactive oxygen species that may result in secondary neuronal damage. Melatonin is an anti-inflammatory and antioxidant agent, and it has been reported to exert neuroprotection through the prevention of neuronal death in several models of central nervous system injury. This study aimed to investigate the effect of melatonin on astrocyte activation induced by Traumatic Brain Injury (TBI) in rat hippocampus and dentate gyrus. Methods: Animals were randomly divided into 5 groups; Sham group, TBI group, vehicle group, and melatonin‐treated TBI groups (TBI+Mel5, TBI+Mel20). Immunohistochemical method (GFAP marker) and TUNEL assay were used to evaluate astrocyte reactivity and neuronal death, respectively. Results: The results demonstrated that the astrocyte number was reduced significantly in melatonin‐treated groups compared to the vehicle group. Additionally, based on TUNEL results, melatonin administration noticeably reduced the number of apoptotic neurons in the rat hippocampus and dentate gyrus. Conclusion: In general, our findings suggest that melatonin treatment after brain injury reduces astrocyte reactivity as well as neuronal cell apoptosis in rat hippocampus and dentate gyrus.

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Song, Juhyun, So Mang Kang, Kyoung Min Lee, and Jong Eun Lee. "The Protective Effect of Melatonin on Neural Stem Cell against LPS-Induced Inflammation." BioMed Research International 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/854359.

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Stem cell therapy for tissue regeneration has several limitations in the fact that transplanted cells could not survive for a long time. For solving these limitations, many studies have focused on the antioxidants to increase survival rate of neural stem cells (NSCs). Melatonin, an antioxidant synthesized in the pineal gland, plays multiple roles in various physiological mechanisms. Melatonin exerts neuroprotective effects in the central nervous system. To determine the effect of melatonin on NSCs which is in LPS-induced inflammatory stress state, we first investigated nitric oxide (NO) production and cytotoxicity using Griess reagent assays, LDH assay, and neurosphere counting. Also, we investigated the effect of melatonin on NSCs by measuring the mRNA levels of SOX2, TLX, and FGFR-2. In addition, western blot analyses were performed to examine the activation of PI3K/Akt/Nrf2 signaling in LPS-treated NSCs. In the present study, we suggested that melatonin inhibits NO production and protects NSCs against LPS-induced inflammatory stress. In addition, melatonin promoted the expression of SOX2 and activated the PI3K/Akt/Nrf2 signaling under LPS-induced inflammation condition. Based on our results, we conclude that melatonin may be an important factor for the survival and proliferation of NSCs in neuroinflammatory diseases.

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Alghamdi, Badrah S. "Protective Efffects of Melatonin in Corpus Callosum Astrocytes during Ischemia in Transgenic Mice." Saudi Journal of Internal Medicine 8, no. 1 (June 30, 2018): 13–23. http://dx.doi.org/10.32790/sjim.2018.8.1.3.

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Objective: Stroke is a leading cause of adult death and disability worldwide. Around 80% of all stroke cases are classed as ischemic stroke, which affects both gray and white matter brain regions. During ischemia, reactive oxygen species are generated and initiate multiple damaging processes such as lipid peroxidation, mitochondrial dysfunction, blood–brain barrier damage and brain edema. Melatonin is a potent antioxidant which can act as a direct oxygen species scavenger. Melatonin can also act at receptors (melatonin receptor 1 and 2), which are expressed in the nervous system cells including astrocytes. Methods: Using live cell imaging of transgenic mice, the viability of astrocytes in the corpus callosum of adult brain sections was monitored during a standard 60 minutes period of modeled ischemia (oxygen-glucose deprivation) and 30 minutes of reperfusion in 8 groups; Control, artificial cerebrospinal fluid + Melatonin, oxygen-glucose deprivation, oxygen-glucose deprivation + Melatonin, oxygen-glucose deprivation + Melatonin + Luzindole (a nonselective melatonin receptor antagonist), oxygen-glucose deprivation + Luzindole, oxygen-glucose deprivation + Melatonin + propionamidotetralin (a selective melatonin receptor 2 antagonist), and oxygen-glucose deprivation + propionamidotetralin. Results: Addition of melatonin significantly reduced the level of astrocyte death during oxygen-glucose deprivation from 71.94% ± 1.45 to 37.84% ± 1.9; p < 0.0001. This protective effect was blocked by luzindole or propionamidotetralin. Following known scoring categories for glial injury, ultrastructural morphology confirmed the protective effect of melatonin against acute ischemic injury in the white matter glial cells. Conclusion: Melatonin is a promising neuroprotective agent during white matter ischemia.

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Tamtaji, Omid Reza, Naghmeh Mirhosseini, Russel J. Reiter, Abolfazl Azami, and Zatollah Asemi. "Melatonin, a calpain inhibitor in the central nervous system: Current status and future perspectives." Journal of Cellular Physiology 234, no. 2 (August 26, 2018): 1001–7. http://dx.doi.org/10.1002/jcp.27084.

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BRISMAR, KERSTIN, BRITTA HYLANDER, KEITH ELIASSON, STEPHAN RÖSSNER, and LENNART WETTERBERG. "Melatonin Secretion Related to Side-effects of β-Blockers from the Central Nervous System." Acta Medica Scandinavica 223, no. 6 (April 24, 2009): 525–30. http://dx.doi.org/10.1111/j.0954-6820.1988.tb17690.x.

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Viswanathan, Mohan, Raimo Hissa, and John C. George. "Suppression of sympathetic nervous system by short photoperiod and melatonin in the Syrian hamster." Life Sciences 38, no. 1 (January 1986): 73–79. http://dx.doi.org/10.1016/0024-3205(86)90277-8.

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Korshnyak, Volodymyr O., and Tetyana A. Donnik. "Rehabilitation of Patients with Long-Term Complications of Mild Closed Traumatic Brain Injuries Using Sensory Deprivation." Acta Balneologica 62, no. 4 (2020): 216–20. http://dx.doi.org/10.36740/abal202004103.

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Introduction: This study’s primary goal was to develop and implement a new non-pharmacological method of therapy to increase the effectiveness of rehabilitation treatment of patients with long-term complications of mild closed traumatic brain injuries. Material and Methods: We examined 100 patients with complications of mild closed traumatic brain injuries in the stage of decompensation. We studied the dynamics of subjective and objective neurological symptoms, vegetative indices (vegetative tonus, vegetative responsiveness, vegetative provisioning), and neuro mediators levels (adrenaline, noradrenaline, serotonin, dopamine, and melatonin) before and after sensory deprivation. Results: During rehabilitation, we observed the positive changes in neurological status as well as in the balance restoration of the nervous system and the neurohormonal normalization of the sympathoadrenal system. It contributed to a more adequate generalized adaptive response of the body. After a series of rehabilitation procedures, the difference between the maximal and control markers of melatonin excretion significantly decreased, which might confirm the evidence of normalization of the processes’ rhythmicity and vital functions, as well as the improvement of complex neuroprotection. Also, the normalization of melatonin excretion in patients was associated with sleep improvement, decreased intensity of the headache syndromes, and increased activity and ability to act. Conclusions: Long-term complications of mild closed traumatic brain injury develop due to activity imbalance of supratentorial structures of the vegetative nervous system, desynchronization of the cortex’s activity, and desynchronization of humoral mechanisms of vegetative activity realization. The use of sensory deprivation promotes much faster rehabilitation of this group of patients, reduces the pharmacological burden on the patient’s body, and improves the brain system’s functioning.

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Sjöblom, Markus, Bengt Säfsten, and Gunnar Flemström. "Melatonin-induced calcium signaling in clusters of human and rat duodenal enterocytes." American Journal of Physiology-Gastrointestinal and Liver Physiology 284, no. 6 (June 1, 2003): G1034—G1044. http://dx.doi.org/10.1152/ajpgi.00500.2002.

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The amount of melatonin present in enterochromaffin cells in the alimentary tract is much higher than that in the central nervous system, and melatonin acting at MT2receptors mediates neural stimulation of mucosal HCO[Formula: see text]secretion in duodenum in vivo. We have examined effects of melatonin and receptor ligands on intracellular free calcium concentration ([Ca2+]i) signaling in human and rat duodenal enterocytes. Clusters of interconnecting enterocytes (10–50 cells) were isolated by mild digestion (collagenase/dispase) of human duodenal biopsies or rat duodenal mucosa loaded with fura-2 AM and attached to the bottom of a temperature-controlled perfusion chamber. Clusters provided viable preparations and respond to stimuli as a syncytium. Melatonin and melatonin receptor agonists 2-iodo- N-butanoyl-5-methoxytryptamine and 2-iodomelatonin (1.0–100 nM) increased enterocyte [Ca2+]i, EC50 of melatonin being 17.0 ± 2.6 nM. The MT2 receptor antagonists luzindole and N-pentanoyl-2-benzyltryptamine abolished the [Ca2+]i responses. The muscarinic antagonist atropine (1.0 μM) was without effect on basal [Ca2+]i and did not affect the response to melatonin. In the main type of response, [Ca2+]i spiked rapidly and returned to basal values within 4–6 min. In another type, the initial rise in [Ca2+]i was followed by rhythmic oscillations of high amplitude. Melatonin-induced enterocyte [Ca2+]i signaling as well as mucosal cell-to-cell communication may be involved in stimulation of duodenal mucosal HCO[Formula: see text] secretion.

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Alarma-Estrany, Pilar, Almudena Crooke, Aránzazu Mediero, Teresa Peláez, and Jesús Pintor. "Sympathetic nervous system modulates the ocular hypotensive action of MT2-melatonin receptors in normotensive rabbits." Journal of Pineal Research 45, no. 4 (November 2008): 468–75. http://dx.doi.org/10.1111/j.1600-079x.2008.00618.x.

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Yu, Xin, Zheng Li, Heyi Zheng, Jeffery Ho, Matthew T. V. Chan, and William Ka Kei Wu. "Protective roles of melatonin in central nervous system diseases by regulation of neural stem cells." Cell Proliferation 50, no. 2 (December 12, 2016): e12323. http://dx.doi.org/10.1111/cpr.12323.

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Kato, Kimitoshi, Ichiro Murai, Satoshi Asai, Yasuo Takahashi, Yoshiaki Matsuno, Sachiko Komuro, Hanzo Kurosaka, Ariyoshi Iwasaki, Koichi Ishikawa, and Yasuyuki Arakawa. "Central nervous system action of melatonin on gastric acid and pepsin secretion in pylorusligated rats." NeuroReport 9, no. 11 (August 1998): 2447–50. http://dx.doi.org/10.1097/00001756-199808030-00004.

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Kato, Kimitoshi, Ichiro Murai, Satoshi Asai, Yasuo Takahashi, Yoshiaki Matsuno, Sachiko Komuro, Hanzo Kurosaka, Ariyoshi Iwasaki, Koichi Ishikawa, and Yasuyuki Arakawa. "Central nervous system action of melatonin on gastric acid and pepsin secretion in pylorusligated rats." NeuroReport 9, no. 17 (December 1998): 3989–92. http://dx.doi.org/10.1097/00001756-199812010-00040.

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Hoover, P. A., M. K. Vaughan, J. C. Little, and R. J. Reiter. "N-Methyl-d-aspartate does not prevent effects of melatonin on the reproductive and thyroid axes of male Syrian hamsters." Journal of Endocrinology 133, no. 1 (April 1992): 51–58. http://dx.doi.org/10.1677/joe.0.1330051.

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ABSTRACT The reproductive and thyroid status of male Syrian hamsters maintained on long days (14 h light, 10 h darkness) were assessed after 10 weeks of daily injections of pharmacological doses of melatonin (25 μg s.c.) and/or N-methyl-dl-aspartic acid (NMDA, 0·025–6 mg i.p.), a compound with receptor sites in the central nervous system which are known to affect reproduction. Melatonin given during the late light phase decreased reproductive organ weights and levels of serum and pituitary prolactin and serum thyroxine (T4); these results are similar to published reports on the effects of chronic short photoperiod treatment of this species. Reproductive organ weights, T4 levels and values for prolactin did not differ significantly between groups receiving only melatonin and those receiving NMDA in addition to melatonin; likewise these variables did not differ significantly between groups receiving only either NMDA or saline. NMDA alone and in combination with melatonin increased serum tri-iodothyronine (T3). The brown adipose tissue enzyme T4 5′-deiodinase demonstrated an increased activity in the presence of NMDA, with the lowest dosage eliciting the most significant effect. Previous studies have demonstrated that NMDA reverses the reproductive effects of short photoperiod. The results of this study show that NMDA is incapable of preventing the inhibitory reproductive effects of exogenously administered melatonin. These observations are consistent with the proposal for a site of action for NMDA on neural regions more proximal than those altered by melatonin; alternatively, NMDA may interfere with neurotransmitter actions in the pathway controlling melatonin production. Journal of Endocrinology (1992) 133, 51–58

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Villela, Darine, Victoria Fairbanks Atherino, Larissa de Sá Lima, Anderson Augusto Moutinho, Fernanda Gaspar do Amaral, Rafael Peres, Thais Martins de Lima, et al. "Modulation of Pineal Melatonin Synthesis by Glutamate Involves Paracrine Interactions between Pinealocytes and Astrocytes through NF-κB Activation." BioMed Research International 2013 (2013): 1–14. http://dx.doi.org/10.1155/2013/618432.

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The glutamatergic modulation of melatonin synthesis is well known, along with the importance of astrocytes in mediating glutamatergic signaling in the central nervous system. Pinealocytes and astrocytes are the main cell types in the pineal gland. The objective of this work was to investigate the interactions between astrocytes and pinealocytes as a part of the glutamate inhibitory effect on melatonin synthesis. Rat pinealocytes isolated or in coculture with astrocytes were incubated with glutamate in the presence of norepinephrine, and the melatonin content, was quantified. The expression of glutamate receptors, the intracellular calcium content and the NF-κB activation were analyzed in astrocytes and pinealocytes. TNF-α's possible mediation of the effect of glutamate was also investigated. The results showed that glutamate's inhibitory effect on melatonin synthesis involves interactions between astrocytes and pinealocytes, possibly through the release of TNF-α. Moreover, the activation of the astrocytic NF-κB seems to be a necessary step. In astrocytes and pinealocytes, AMPA, NMDA, and group I metabotropic glutamate receptors were observed, as well as the intracellular calcium elevation. In conclusion, there is evidence that the modulation of melatonin synthesis by glutamate involves paracrine interactions between pinealocytes and astrocytes through the activation of the astrocytic NF-κB transcription factor and possibly by subsequent TNF-αrelease.

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Leitner, Claudia, and Timothy J. Bartness. "Distributed Forebrain Sites Mediate Melatonin-Induced Short-Day Responses in Siberian Hamsters." Endocrinology 151, no. 7 (May 5, 2010): 3133–40. http://dx.doi.org/10.1210/en.2010-0002.

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The pineal hormone melatonin (MEL) is the key initiator in regulating seasonal photoperiodic responses; however, the central sites that mediate short day (SD) winter-like responses, such as testicular regression and decreases in white adipose tissue (WAT) mass, by Siberian hamsters are not precisely known. WAT is innervated by the sympathetic nervous system, and several forebrain sites that are part of the sympathetic nervous system outflow to WAT coexpress MEL1a receptor mRNA [e.g. suprachiasmatic nucleus, subzona incerta (SubZi), dorsomedial nucleus of the hypothalamus, nucleus reunions and paraventricular nuclei of the thalamus]. We tested the involvement of these sites in MEL-triggered SD responses. A long duration, SD-like MEL signal was applied site specifically for 5 wk, with sc and third ventricle MEL application serving as positive controls. Whereas SD MEL signals delivered to each of these sites were able to induce testicular regression, all but the paraventricular nuclei of the thalamus also trigger SD-induced decreases in body mass. Third ventricle, sc, suprachiasmatic nucleus, or SubZi MEL application also decreased WAT mass, and only sc and SubZi MEL application decreased food intake. Collectively these data suggest a distributed system of MEL-sensitive brain sites sufficient to mediate these SD responses, the redundancy of which suggests its importance for appropriate seasonal responses critical for overwintering.

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Flemström, Gunnar, and Markus Sjöblom. "Epithelial Cells and Their Neighbors. II. New perspectives on efferent signaling between brain, neuroendocrine cells, and gut epithelial cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 289, no. 3 (September 2005): G377—G380. http://dx.doi.org/10.1152/ajpgi.00093.2005.

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Surface sensory enteroendocrine cells are established mucosal taste cells that monitor luminal contents and provide an important link in transfer of information from gut epithelium to the central nervous system. Recent studies now show that these cells can also mediate efferent signaling from the brain to the gut. Centrally elicited stimulation of vagal and sympathetic pathways induces release of melatonin, which acts at MT2 receptors to increase mucosal electrolyte secretion. Psychological factors as well mucosal endocrine cell hyperplasia are implicated in functional intestinal disorders. Central nervous influence on the release of transmitters from gut endocrine cells offers an exciting area of future gastrointestinal research with a clinical relevance.

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Journal articles on the topic 'Melatonin. Nervous system'

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