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Letteratura scientifica selezionata sul tema "Melatonin. Nervous system"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 16 febbraio 2022

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Articoli di riviste sul tema "Melatonin. Nervous system"

Hardeland, Rudiger. "Melatonin Metabolism in the Central Nervous System." Current Neuropharmacology 8, no. 3 (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 (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 (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 (2016): 5–15. http://dx.doi.org/10.37897/rjn.2016.1.1.

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Abstract (sommario):

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 (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 (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 (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 (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, et al. "Melatonin—A Potent Therapeutic for Stroke and Stroke-Related Dementia." Antioxidants 9, no. 8 (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 (1998): 359–84. http://dx.doi.org/10.1016/s0301-0082(98)00052-5.

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Più fonti

Tesi sul tema "Melatonin. Nervous system"

Maharaj, Deepa Sukhdev. "An investigation into the physico-chemical and neuroprotective properties of melatonin and 6-hydroxymelatonin." Thesis, Rhodes University, 2003. http://eprints.ru.ac.za/71/.

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Parmar, Paresh H. "An investigation into the possible neuroprotective role of melatonin in copper-loading." Thesis, Rhodes University, 2001. http://hdl.handle.net/10962/d1003261.

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Copper is an extremely toxic metal in biological systems and thus, its availability to the system, must be effectively and efficiently controlled. Copper is vital for life, as it is essential for critical enzymes in biological systems. It is free copper in the biological systems that is toxic, as free copper induces free radical generation, which disrupts lipid membranes, interacts with DNA causing mutations, and eventually leads to cell death. Wilson’s disease is a inherited copper disease, which results in hepatolenticular disease. Copper is unable to be excreted, and thus accumulates, eventually spilling over into the bloodstream from the liver, and “poisons” the patient. The Wilson’s disease patient leads a short life, due to neurological and hepatological problems. There is no cure for Wilson’s disease, only chelation therapy using potent chelators such as penicillamine and EDTA. Zinc, in high doses, can be used to compete with copper absorption. This has proved to be the only successful therapy at present. This study investigates the possible use of melatonin as a copper binder/chelator. Melatonin has been shown to interact with copper in vitro. By binding/chelating to copper, melatonin may inhibit copper-induced free radical generation, and thus prevent copper from interacting with DNA to cause mutations and act as a cytotoxin. In vivo studies on copper (2mg/kg) administered for 2-weeks and 6-weeks were carried out on Wistar rats. The potential of melatonin (12mg/kg) to prevent copper-induced cellular damage was investigated. The results indicate that melatonin does not protect the lipid membranes from copper-induced lipid peroxidation. In vitro investigations using 1mM, 5mM and 10mM copper and 5mM melatonin, show that melatonin prevents copper-induced lipid peroxidation at a copper concentration of 1mM (p<0.001). The 5mM and 10mM copper induces less lipid peroxidation, compared to the 1mM copper. It has been reported that metal ions, antioxidants and chelating agents can influence peroxide decomposition during the assay. Melatonin (5mM) administration does not significantly prevent copper-induced lipid peroxidation at 5mM and 10mM copper. It is possible that due to melatonin’s relatively low concentration, it is unable to inhibit lipid peroxidation induced by the copper. The chemical nature of the interaction between melatonin and copper was also investigated, using NMR, IR and electrochemistry techniques. The NMR and IR techniques show that melatonin coordinates with Cu²⁺ and not Cu¹⁺, at the carbonyl group of melatonin. The electrochemistry experiments using cyclic voltammetry and adsorptive stripping voltammetry, show that melatonin forms a strong bond with Cu¹⁺. Cu²⁺ prefers binding to oxygen, and that is clearly seen in the NMR and IR. Cu¹⁺ prefers binding to nitrogen and then oxygen, and this is seen in the electrochemistry, as Cu¹⁺ is forced to bind through one of the nitrogens on the melatonin. Previously, it has been shown that melatonin binds/chelates with Cu²⁺. Histochemical investigations show that copper administration for 2-weeks and 6-weeks, causes extensive mitochondrial damage in liver and kidney’s proximal convoluted tubule epithelium cells. Melatonin (12mg/kg) co-administration with copper for 2-weeks and 6-weeks did not significantly protect the mitochondria from copper-induced damage. Copper-specific stains (rhodanine, silver sulphide and rubeanic acid) were used to stain liver, brain and kidney tissue samples. Rhodanine and silver sulphide were equally sensitive in staining copper in the 2-week samples, but not at all in the 6-week samples. This could not be explained. Rubeanic acid was ineffective in all samples tested. Thus, it appears that specific copper stains cannot be used in making a definitive diagnosis in cases of copper overload, and that specific copper stains do not always correlate with a high concentration of copper present in tissues. Pineal organ culture was used to determine the effect of copper administration on pineal indole synthesis. Exogenous (³H) tryptophan was administered to the pineal organ cultures, and the level of (³H) pineal indoles synthesised, were measured. Pineals from 2-week and 6-week copper/melatonin treated animals exhibited paradoxical 5- methoxytryptophol (ML) levels, as compared to the 2-week and 6-week copper treated animals. The 2-week copper/melatonin administered animals, showed a decrease in the ML level (p<0.01), and the copper/melatonin administered for 6-weeks, showed an increase in the ML levels (p<0.01). This indicates that melatonin interacts with the HIOMT enzyme. Pineals from 6-week copper/melatonin treated animals, as compared to the 6-week copper treated animals, showed an increase in N-acetylserotonin levels. This indicates that melatonin prevents the inhibition of the NAT enzyme. The final experiment was to determine in vitro, the effect of Cu²⁺ and Cu¹⁺ administration, on mitochondrial electron transport chain. Rat liver homogenate was incubated with and solutions of Cu²⁺ (10mM) and Cu¹⁺ (10mM) and melatonin (10mM). Cu²⁺ administration caused an inhibition of the electron transport at t=0 and t=60, whereas Cu¹⁺ administration at t=0 caused an inhibition of electron transport, but at t=60, Cu¹⁺ administration stimulated electron transport. Melatonin administered with Cu²⁺, resulted in an inhibition of the electron transport chain at t=0 and t=60. The findings of this study indicate that melatonin might have a potentially beneficial effect in copper overloading, by binding/chelating copper.

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Sjöblom, Markus. "The duodenal mucosal bicarbonate secretion : role of melatonin in neurohumoral control and cellular signaling /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. {[distributör], 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3521.

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Kadanthode, Rubina John. "An investigation into the neuroprotective effects of melatonin in a model of rotenone-induced neurodegeneration." Thesis, Rhodes University, 2004. http://hdl.handle.net/10962/d1003241.

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Abstract (sommario):

Parkinson’s disease, one of the most common neurodegenerative disorders associated with ageing, is characterised by abnormal and profound loss of nigrostriatal dopaminergic neurons. The cause of Parkinson’s disease is unknown, but epidemiological studies suggest an association with pesticides and other environmental toxins, and biochemical studies implicate oxidative damage and mitochondrial impairment, particularly at the level of complex I enzyme. Recently, rotenone, a commonly used organic pesticide and a classical inhibitor of mitochondrial complex I has been reported to reproduce the specific features of Parkinson’s disease in rodents. The mitochondrial respiratory chain is one of the most important sites of reactive oxygen species production under physiological conditions. Toxic free radicals have been implicated in a variety of neurodegenerative diseases as well as ageing itself. Melatonin, a secretory product of the pineal gland is a multifaceted free radical scavenger and natural antioxidant. In the present study, the neuroprotective effects of melatonin against the environmental neurotoxin, rotenone was investigated. Initial studies showed that inhibition of mitochondrial complex I enzyme by rotenone induced superoxide radical generation. Melatonin, administered to the rat in vivo and in vitro was able to offer neuroprotection by curtailing the production of superoxide radicals induced by rotenone. Mitochondria, being the major target of rotenone, the effects of melatonin were investigated at the mitochondrial level. Melatonin was able to increase the electron transport chain activity thus preventing the respiratory inhibition by rotenone. The pineal hormone also counteracted the action of rotenone on complex I enzyme. These results suggest melatonin’s ability to potentially limit the free radical generation and thereby modulate the mitochondrial functions. The detection and measurement of lipid peroxidation is the evidence most frequently cited to support the involvement of free radical reactions in toxicology and in human disease. Melatonin also offered significant protection in vivo and in vitro against rotenone induced lipid peroxidation. Since iron plays a major role in oxidative damage and in the progression of Parkinson’s disease, the effect of melatonin on both rotenone and iron induced lipid peroxidation was investigated, the results of which show that melatonin affords protection and this was suggested to be due to its interaction with the rotenone-iron complex that might have formed. Electrochemical studies were further used to characterise the interactions between melatonin, rotenone and iron (III). Melatonin was shown to bind with iron and thus reducing their toxicity. Histological studies were undertaken to assess the effects of melatonin on rotenone induced toxicity on the dopaminergic neurons in the rat brain. Rotenone treated brains showed extensive neuronal damage whereas with melatonin less damage was observed. Rotenone induces apoptosis via reactive oxygen species production and apoptotic cell death has been identified in PD brains. Furthermore, the apoptotic cell death was detected and quantified by the TUNEL staining. Rotenone treated sections showed signs of apoptosis whereas with melatonin, less apoptotic damage was observed. The findings of this study indicate that the neurohormone, melatonin may protect against rotenone-induced neurodegeneration. Since melatonin production falls substantially during ageing, the loss of this antioxidant is theorized to be instrumental in the degenerative processes associated with advanced age. Considering how devastating diseases such as Parkinson’s disease, are to a patient and the patient’s families, the discovery of protective agents are a matter of urgency. Further investigations using the pesticide model will help to determine the involvement of environmental exposure in the pathogenesis of human diseases as well as to test therapeutic strategies for the treatment of such diseases.

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Perreau, Stéphanie Marie. "Control of the daily melatonin rhythm a model of time distribution by the biological clock mediated through the autonomic nervous system /." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2004. http://dare.uva.nl/document/73034.

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Burton, Susan Frances. "A study of the effects of the pineal hormone, melatonin, on dopaminergic transmission in the central nervous system of rats." Thesis, Rhodes University, 1990. http://hdl.handle.net/10962/d1001463.

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Dopamine mechanisms in the central nervous system are important in the control of both normal and abnormal motor function. The recent observations in both animal and human studies, that melatonin, the principal hormone of the pineal gland, may have a role in the control of movement and the pathophysiology of movement disorders, have given rise to the concept that melatonin may have a modulatory influence on central dopaminergic neurotransmission. This study makes use of three animal behavioural models as well as a biochemical model of central dopaminergic function to further investigate the concept. Results from studies using the biochemical model, which investigated the effect of melatonin on dopamine and apomorphine stimulation of dopamine-sensitive adenylate cylase, suggest that melatonin is neither a competitive antagonist nor agonist at the D₁ receptor level, although the possibility of physiological stimulation or antagonism is not excluded. In behavioural studies, prior melatonin mg/kg administration (1 and 10 (8M) ip) inhibited apomorphine induced stereotypy and locomotor activity in normal rats, and apomorphine-induced rotational behaviour in 6-hydroxydopamine and quinolinic acid lesioned rats. The possibility that these results may have physiological significance is borne out by the observation that, under enviromental lighting conditions that are associated with raised endogeous melatonin levels, apomorphine- induced stereotypy and locomotor activity is attenuated. The general conclusion is that melatonin has an inhibitory influence on central nervous system dopaminergic function, suggesting therefore, that the pineal gland and melatonin may have a role in the pathophysiology and treatment of movement and behavioural disorders associated with dopaminergic dysfunction

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Lenz, Stéphanie. "Control of the daily melatonin rhythm : A model of time distribution by the biological clock mediated through the autonomic nervous system." Université Louis Pasteur (Strasbourg) (1971-2008), 2004. https://publication-theses.unistra.fr/public/theses_doctorat/2004/LENZ_Stephanie_2004.pdf.

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Chez les Mammifères, les rythmes circadiens, présentant une rythmicité endogène proche de 24h sont sous le contrôle d'une horloge interne située dans les Noyaux Suprachiasmatiques de l'hypothalamus (NSC). Afin de mieux comprendre la distribution du message temps par les NSC, nous avons étudié spécifiquement le contrôle du rythme journalier de sécrétion de mélatonine, hormone sécrétée de nuit par la glande pinéale, partant du postulat selon lequel les NSC contrôleraient ce rythme en utilisant, pendant la journée, un signal inhibiteur de nature GABAergique pour inhiber la voie polysynaptique reliant les Noyaux paraventriculaires de l'hypothalamus (PVN) à la glande pinéale. Nos premiers travaux ont révélé, par lésions thermiques des différents noyaux intéressés, un rôle de simple relais de l'information pour les PVN, ainsi qu'une action inhibitrice des NSC sur la synthèse de mélatonine de jour associée à une action stimulatrice nocturne. A l'aide de la technique de microdialyse intracérébrale multiple, nous avons ensuite pu confirmer, in vivo, que l'activité neuronale nocturne des NSC était cruciale pour une stimulation nocturne de synthèse de mélatonine. De plus, un rôle important du neurotransmetteur glutamate a pu être montré pour cette action stimulatrice. Nous avons également montré que la chute de sécrétion de mélatonine en fin de nuit était due à une augmentation de sécrétion GABAergique par les NSC associée soit à la disparition du signal stimulateur soit à l'apparition d'un second signal inhibiteur. Par ailleurs, en corrélant l'expression neuronale des gènes de l'horloge Per1 et Per2 et la sécrétion de vasopressine par les NSC, nous avons révélé une régionalisation fonctionnelle des NSC. Ensemble, les résultats de cette thèse ont permis de réactualiser le concept du contrôle du rythme journalier de mélatonine par l'horloge biologique, exemple de moyen de distribution du message temps au reste de l'organisme via le système nerveux autonome
In mammals, circadian rhythms, i. E. Showing an endogenous rhythmicity close to 24h are under the control of a master biological clock, located in the suprachiasmatic nucleus of the hypothalamus (SCN). In order to further understand the mechanisms of time distribution by the SCN, we specifically studied the control of the daily secretion of melatonin, hormone strictly produced at night by the pineal gland, with the initial hypothesis that the SCN controls the daily rhythm of melatonin synthesis by imposing during daytime an inhibitory signal of GABAergic nature onto the polysynaptic pathway connecting the Paraventricular Nucleus of the hypothalamus (PVN) to the pineal gland. By lesioning or removing the different nuclei involved in this pathway, our first study revealed a simple role of information-relay for the PVN, as well as a combined inhibitory and stimulatory role for the SCN during the day and the night respectively. Using the multiple intracerebral microdialysis technique, we were then able to confirm in vivo that the SCN nocturnal activity is crucial for a nocturnal stimulation of melatonin synthesis and we showed as well that glutamatergic transmission is responsible for such a stimulatory action onto the melatonin synthesis. In addition, we revealed that the early morning drop of melatonin synthesis is due to the association of an increased GABAergic secretion derived by the SCN and either the disappearance of the stimularory signal or the appearance of a second inhibitory signal. Furthermore, correlating the neuronal expression of the clock genes Per1 and Per2 and the SCN vasopressin secretion, we revealed a clear functional compartmentalisation of the SCN. Together these results helped re-actualising the concept of the control of the daily rhythm of melatonin synthesis by the biological clock, which is a great example of time distribution to the rest of the organism via the autonomic nervous system

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Sommansson, Anna. "Regulation of Duodenal Mucosal Barrier Function and Motility : The Impact of Melatonin." Doctoral thesis, Uppsala universitet, Fysiologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-209669.

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The duodenal mucosa is regularly exposed to acid, digestive enzymes and ingested noxious agents. It is thus critical to maintain a protective barrier to prevent the development of mucosal injury and inflammation, which are often observed in situations when barrier function is impaired. The rate of mucosal bicarbonate secretion, the regulation of epithelial paracellular permeability and motility are each key components of duodenal barrier function. The hormone melatonin is present in high levels in the gastrointestinal tract and it has been hypothesized that melatonin exerts protective properties. This thesis aims to investigate the impact of exogenous melatonin on the regulation of duodenal barrier function and motility in anesthetized rats in vivo. In addition, duodenal tissue was examined histologically and the expression levels of tight junction proteins and melatonin receptors were assessed with qRT-PCR. It was found that melatonin stimulated mucosal bicarbonate secretion and decreased basal paracellular permeability. Exposing the duodenal mucosa to the well-characterized barrier breaker ethanol increased mucosal bicarbonate secretion, paracellular permeability and motility. Omission of luminal Clˉ abolished, while pretreatment with a nicotinic receptor antagonist reduced, the ethanol-induced bicarbonate secretion suggesting that the secretory response to ethanol is meditated via Clˉ/HCO3ˉexchangers and enteric neural pathways. Melatonin reduced the ethanol-induced increases in paracellular permeability and motility either when injected intravenously or when administered in drinking water for two weeks. The actions of melatonin were abolished by the melatonin receptor antagonist luzindole and by nicotinic acetylcholine receptor inhibition. Two weeks oral administration of melatonin up-regulated the expression levels of melatonin receptors, down-regulated the expression of ZO-3 while the expression of ZO-1, ZO-2, claudin 2-4, occludin and myosin light chain kinase were unaffected. Superficial epithelial changes in a few villi were seen in response to ethanol exposure, an effect that was histologically unchanged by melatonin pretreatment. In conclusion, the results suggest that melatonin plays an important role in the neurohumoral regulation of gastrointestinal mucosal barrier function and motility via receptor- and enteric neural-dependent pathways in vivo in rats. Melatonin might be a candidate for treatment of barrier dysfunction in humans.

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Lack, Barbara Anne. "Metal interactions with neural substrates and their role in neurodegeneration." Thesis, Rhodes University, 2003. http://hdl.handle.net/10962/d1005709.

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"Life" may be characterized as a controlled stationary flow equilibrium, maintained by energy consuming chemical reactions. The physiological functioning of these life systems include at least 28 of the elements isolated on the periodic table thus far, most of which are metals. However, as with Paracelsus Principle: "The dose makes the poison", there exists a definite link between metal levels, essential and toxic, and the onset of neurodegenerative diseases. The economic costs of brain dysfunction are enormous, but this pales in comparison to the staggering emotional toll on the victims themselves and their families. In an attempt to improve the understanding of the causes of neurodegeneration, this study focuses on one potential aspect: the possible link between metals and neurotransmitter homeostasis utilising a variety of electronanalytical techniques. Adsorptive cathodic stripping voltammetry was employed to investigate the binding affinities and complex formation of melatonin and its precursor serotonin with calcium, potassium, sodium, lithium and aluminium. The results showed that all the metals studied formed complexes with both pineal indoleamines. However, the stability and affmity of the ligands toward the various metals varied greatly. The study suggests a further role for melatonin, that of metalloregulator and possible metal detoxifier in the brain, the in vivo studies which followed will further substantiate this notion. This research additionally focused on the cholinergic system, in particular acetylcholine complex formation studies with mercury, lead, cadmium, copper and zinc using the adsorptive cathodic stripping voltammetry method. The formation and characterisation of a solid mercury-acetylcholine complex lent further strength to the in situ electrochemical complex formation observed. The results showed the preference of acetylcholine for environmentally toxic heavy metals (such as Cd²⁺) over those divalent cations that occur naturally in the body. The possible metalloregulatory role melatonin played in the three brain regIOns: cerebellum, cortex and corpus striatum of male Wistar rats was studied as an in vivo extension of the earlier in vitro studies. Anodic stripping voltammetry was employed to detect metal levels present. The results showed that daily injections of melatonin was responsible for significantly decreasing copper(I), cadmium(II) and lead(II) levels in various regions of the rat brain of those animals that had undergone a pinealectomy in comparison to the saline injected group having undergone the same treatment. Histological and electrochemical stripping techniques were applied to investigate the implications of high A1³⁺ levels in the brain regions, particularly the hippocampus. Melatonin showed signs of promise in indirect symptom alleviation and by significantly decreasing A1³⁺ levels in rats that had been dosed with melatonin prior to A1³⁺ treatments in comparison with the control groups. Finally a preliminary study outlining a method for the production of a calcium selective microelectrode was undertaken. Further work is still needed to optimise the microelectrode production as well as its possible applications. However, whilst the overall conclusions of this entire multidisciplinary study may indeed only be in effect one piece of a very large puzzle on neurodegenerative diseases, this piece will no doubt serve as a building block for further ideas and work in this field.

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Sjöblom, Markus. "The Duodenal Mucosal Bicarbonate Secretion : Role of Melatonin in Neurohumoral Control and Cellular Signaling." Doctoral thesis, Uppsala University, Physiology, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3521.

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Abstract (sommario):

The duodenal lumen is exposed to aggressive factors with a high potential to cause damage to the mucosa. Bicarbonate secretion by the duodenal mucosa is accepted as the primary important defense mechanism against the hydrochloric acid intermittently expelled from the stomach.

The present thesis concerns the influence of the central nervous system and the effects of the hormone melatonin on bicarbonate secretion in anesthetized rats in vivo. Effects of melatonin on intracellular calcium signaling by duodenal enterocyte in vitro were examined in tissues of both human and rat origin. The main findings were as follows:

Melatonin is a potent stimulant of duodenal mucosal bicarbonate secretion and also seems to be involved in the acid-induced stimulation of the secretion. Stimulation elicited in the central nervous system by the α1-adrenoceptor agonist phenylephrine induced release of melatonin from the intestinal mucosa and a four-fold increase in alkaline secretion. The melatonin antagonist luzindole abolished the duodenal secretory response to administered melatonin and to central nervous phenylephrine but did not influence the release of intestinal melatonin. Central nervous stimulation was also abolished by synchronous ligation of the vagal trunks and the sympathetic chains at the sub-laryngeal level.

Melatonin induced release of calcium from intracellular stores and also influx of extracellular calcium in isolated duodenal enterocytes. Enterocytes in clusters functioned as a syncytium.

Overnight fasting rapidly and profoundly down-regulated the responses to the duodenal secretagogues orexin-A and bethanechol but not those to melatonin or vasoactive intestinal polypeptide.

In conclusion, the results strongly suggest that intestinal melatonin plays an important role in central nervous elicited stimulation of duodenal mucosal bicarbonate secretion. Sensitivity of this alkaline secretion to some peripheral stimulators markedly depends on the feeding status.

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Più fonti

Libri sul tema "Melatonin. Nervous system"

Switzerland) International Congress Isnim 1999 (Lugano. Neuroimmunomodulation: Perspectives at the New Milennium (Annals of the New York Academy of Sciences). New York Academy of Sciences, 2000.

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Capitoli di libri sul tema "Melatonin. Nervous system"

Dubocovich, M. L. "Melatonin Receptors in the Central Nervous System." In Advances in Experimental Medicine and Biology. Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4684-5952-4_23.

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Smith, J. A. "Biochemical and Behavioural Studies of Melatonin." In Circadian Rhythms in the Central Nervous System. Palgrave Macmillan UK, 1985. http://dx.doi.org/10.1007/978-1-349-07837-0_1.

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Arendt, Josephine. "The Pineal Hormone Melatonin in Seasonal and Circadian Rhythms." In Circadian Rhythms in the Central Nervous System. Palgrave Macmillan UK, 1985. http://dx.doi.org/10.1007/978-1-349-07837-0_2.

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Checkley, S. A., C. Thompson, C. Franey, and J. Arendt. "Effects of Desipramine on Melatonin and Cortisol in Normal and Depressed Subjects." In Circadian Rhythms in the Central Nervous System. Palgrave Macmillan UK, 1985. http://dx.doi.org/10.1007/978-1-349-07837-0_27.

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Dubocovich, M. L. "Pharmacology and Function of Melatonin Receptors in the Mammalian Central Nervous System." In Serotonin. Palgrave Macmillan UK, 1989. http://dx.doi.org/10.1007/978-1-349-10114-6_32.

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Pang, S. F., H. Yuan, Z. H. Yu, et al. "Melatonin Binding Sites in the Nervous and Immune Systems." In Role of Melatonin and Pineal Peptides in Neuroimmunomodulation. Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3756-4_11.

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Anderson, George, and Michael Maes. "Alpha 7 Nicotinic Receptor Agonist Modulatory Interactions with Melatonin: Relevance not only to Cognition, but to Wider Neuropsychiatric and Immune Inflammatory Disorders." In Frontiers in Clinical Drug Research- Central Nervous System. BENTHAM SCIENCE PUBLISHERS, 2016. http://dx.doi.org/10.2174/9781681081892116020006.

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FRASCHINI, FRANCO, and BOJIDAR STANKOV. "Distribution of the Melatonin Receptor in the Central Nervous System of Vertebrates. Kinetic Parameters and Signal Transduction Pathways." In Light and Biological Rhythms in Man. Elsevier, 1993. http://dx.doi.org/10.1016/b978-0-08-042279-4.50012-1.

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Kitzen, Jan M. "Use of Benzodiazepines and Z-Drugs in the Geriatric Population." In The Benzodiazepines Crisis. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780197517277.003.0004.

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Abstract (sommario):

The benzodiazepine (BZD) class of drugs has proven to be a useful addition to therapeutic management of anxiety and sleep disorders in the adult population. However, after many years of experience with BZDs in elderly patients (≥65 years), a large body of evidence indicates that BZDs are no longer recommended for use in this segment of the population, except under special conditions. Several aging-related changes in physiology such as decreases in renal and hepatic function, altered central nervous system function and changes in body composition can lead to impaired excretion of drug, higher plasma levels and accumulation of these drugs in the body. Side effects such as sedation, dizziness, cognitive impairment, and diminished control of gait and balance functions place the elderly at greater risk of various adverse events, especially falls and fractures, compared to younger adults. Another class of drugs, known as Z-drugs is structurally dissimilar from the BZDs but able to bind to GABA_A, receptors making them useful for management of insomnia. These drugs have also been found to pose significant hazards to the elderly and are also not recommended for use in elderly patients. Both of these classes of drugs are currently included in the AGS Beers Criteria^® of potentially inappropriate medications for use in the elderly. Alternative pharmacologic approaches to managing these conditions include use of either serotonin-norepinephrine reuptake inhibitors or buspirone for anxiety and the use of either low doses of doxepin, melatonin, or the melatonin agonist ramelteon for management of insomnia. Cognitive behavioral therapy and other relaxation techniques offer non-pharmacologic approaches to managing these conditions, thereby decreasing the need for prescribing BZDs or Z-drugs in the elderly.

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Yurt, Kıymet Kübra, Elfide Gizem Kıvrak, Gamze Altun, Abit Aktas, Arife Ahsen Kaplan, and Süleyman Kaplan. "Neuroprotective Effects of Melatonin and Omega-3 on the Central Nervous System Exposed to Electromagnetic Fields in the Pre- and Postnatal Periods." In Omega Fatty Acids in Brain and Neurological Health. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-815238-6.00011-0.

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