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Journal articles on the topic 'Serotonin'

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Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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1

Park, K. H., J. P. Long, and J. G. Cannon. "Effects of serotonin1-like receptor agonists on autonomic neurotransmission." Canadian Journal of Physiology and Pharmacology 69, no. 12 (December 1, 1991): 1855–60. http://dx.doi.org/10.1139/y91-274.

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Serotonin1A receptor agonists, 8-hydroxy-2-(di-n-propylamino)tetralin and 10-methyl-11-hydroxyaporphine, inhibited electrical stimulation-induced contraction of the guinea-pig ileum. These agonists also inhibited the pressor and tachycardiac responses to low frequency (0.25 Hz) but not to high frequency (2.0 Hz) electrical stimulation of the sympathetic nervous system in pithed rats. Serotonin1B receptor agonist RU 24969 inhibited pressor and tachycardiac responses to both low and high frequencies of stimulation in pithed rats. In the cat nictitating membrane, serotonin1A receptor agonists did not alter contractions elicited by electrical stimulation (0.1–3.0 Hz). Serotonin not only contracted the cat nicitating membrane but also facilitated contractile responses to low frequency (0.1 – 1.0 Hz) stimulation. The contractile effect of serotonin in the cat nictitating membrane was blunted by bretylium, methysergide, and ketanserin, but not by metoclopramide. The facilitatory effect of serotonin was antagonized by methysergide, but not by ketanserin, pindolol, propranolol, or metoclopramide. These results suggest that serotonin1A receptors modulate autonomic neurotransmission in the guinea-pig ileum and pithed rats, but not in the cat nictitating membrane. Serotonin contracts the cat nictitating membrane via serotonin2 subtypes, while facilitating stimulated contractile responses through the serotonin1-like receptors.Key words: guinea-pig ileum, pithed rats, nictitating membrane, serotonin receptors.

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2

Lippton, H. L., Q. Hao, and A. Hyman. "L-NAME enhances pulmonary vasoconstriction without inhibiting EDRF-dependent vasodilation." Journal of Applied Physiology 73, no. 6 (December 1, 1992): 2432–39. http://dx.doi.org/10.1152/jappl.1992.73.6.2432.

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The purpose of the present study was to determine the influence of NG-nitro-L-arginine methyl ester (L-NAME) on pulmonary vascular responses to endothelium-dependent relaxing factor- (EDRF) dependent and EDRF-independent substances in the pulmonary vascular bed of the anesthetized cat. Because pulmonary blood flow and left atrial pressure were kept constant, changes in lobar arterial pressure directly reflect changes in pulmonary vascular resistance. When pulmonary vasomotor tone was actively increased by intralobar infusion of U-46619, intralobar bolus injections of acetylcholine, bradykinin, serotonin, and 5-carboxyamidotryptamine (a serotonin1A receptor agonist) decreased lobar arterial pressure in a dose-related manner. The pulmonary vasodilator response to serotonin, but not to 5-carboxyamidotryptamine, acetylcholine, and bradykinin, was significantly decreased by L-NAME (100 mg/kg i.v.). Administration of ritanserin (0.5 mg/kg i.v.), but not L-arginine (1 g/kg i.v. with 60 mg.kg-1 x min-1 i.v. infusion), reversed the inhibitory effects of L-NAME on the pulmonary vasodilator response to serotonin and abolished the enhanced pulmonary vasoconstrictor response to (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminoproprane hydrochloride (a serotonin2 receptor agonist) after L-NAME administration. In conclusion, the present experiments suggest that L-NAME inhibits the pulmonary vasodilator response to serotonin by increasing the sensitivity of serotonin2 receptor-mediated vasoconstriction and not by inhibiting EDRF formation. Because the pulmonary vasodilator responses to bolus administration of acetylcholine and bradykinin were not inhibited by L-NAME, these data suggest that L-NAME does not appear to be an adequate probe to study the role of endogenous EDRF in the adult feline pulmonary vascular bed in vivo.

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3

Balakrishna, Pragathi, Sagila George, Hassan Hatoum, and Sarbajit Mukherjee. "Serotonin Pathway in Cancer." International Journal of Molecular Sciences 22, no. 3 (January 28, 2021): 1268. http://dx.doi.org/10.3390/ijms22031268.

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Serotonin (5-hydroxytryptamine, 5-HT) is a biogenic monoamine produced from the essential amino acid tryptophan. Serotonin’s role as a neurotransmitter in the central nervous system and a motility mediator in the gastrointestinal tract has been well defined, and its function in tumorigenesis in various cancers (gliomas, carcinoids, and carcinomas) is being studied. Many studies have shown a potential stimulatory effect of serotonin on cancer cell proliferation, invasion, dissemination, and tumor angiogenesis. Although the underlying mechanism is complex, it is proposed that serotonin levels in the tumor and its interaction with specific receptor subtypes are associated with disease progression. This review article describes serotonin’s role in cancer pathogenesis and the utility of the serotonin pathway as a potential therapeutic target in cancer treatment. Octreotide, an inhibitor of serotonin release, is used in well-differentiated neuroendocrine cancers, and the tryptophan hydroxylase (TPH) inhibitor, telotristat, is currently being investigated in clinical trials to treat patients with metastatic neuroendocrine tumors and advanced cholangiocarcinoma. Several in vitro studies have shown the anticancer effect of 5-HT receptor antagonists in various cancers such as prostate cancer, breast cancer, urinary bladder, colorectal cancer, carcinoid, and small-cell lung cancer. More in vivo studies are needed to assess serotonin’s role in cancer and its potential use as an anticancer therapeutic target. Serotonin is also being evaluated for its immunoregulatory properties, and studies have shown its potential anti-inflammatory effect. Therefore, it would be of interest to explore the combination of serotonin antagonists with immunotherapy in the future.

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4

Sarkar, Parijat, Kaleeckal G. Harikumar, Satinder S. Rawat, Sanjib Das, Tushar K. Chakraborty, and Amitabha Chattopadhyay. "Environment-Sensitive Fluorescence of 7-Nitrobenz-2-oxa-1,3-diazol-4-yl (NBD)-Labeled Ligands for Serotonin Receptors." Molecules 26, no. 13 (June 24, 2021): 3848. http://dx.doi.org/10.3390/molecules26133848.

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Serotonin is a neurotransmitter that plays a crucial role in the regulation of several behavioral and cognitive functions by binding to a number of different serotonin receptors present on the cell surface. We report here the synthesis and characterization of several novel fluorescent analogs of serotonin in which the fluorescent NBD (7-nitrobenz-2-oxa-1,3-diazol-4-yl) group is covalently attached to serotonin. The fluorescent ligands compete with the serotonin1A receptor specific radiolabeled agonist for binding to the receptor. Interestingly, these fluorescent ligands display a high environmental sensitivity of their fluorescence. Importantly, the human serotonin1A receptor stably expressed in CHO-K1 cells could be specifically labeled with one of the fluorescent ligands with minimal nonspecific labeling. Interestingly, we show by spectral imaging that the NBD-labeled ligand exhibits a red edge excitation shift (REES) of 29 nm when bound to the receptor, implying that it is localized in a restricted microenvironment. Taken together, our results show that NBD-labeled serotonin analogs offer an attractive fluorescent approach for elucidating the molecular environment of the serotonin binding site in serotonin receptors. In view of the multiple roles played by the serotonergic systems in the central and peripheral nervous systems, these fluorescent ligands would be useful in future studies involving serotonin receptors.

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5

Lee, Jeon Lo. "A Comparison of Genetic versus Non-Genetic Contribution of Serotonin to Suicide." Science Insights 43, no. 1 (July 31, 2023): 995–1002. http://dx.doi.org/10.15354/si.23.re611.

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Suicide is a complex and multifaceted public health issue that has been intensively studied to identify its contributing factors. Serotonin, a neurotransmitter essential for affective regulation and mood control, has been linked to suicidal propensity. Understanding the relative contribution of serotonin’s genetic versus non-genetic influences is essential for the development of effective preventive measures, given that the etiology of suicide involves both genetic and non-genetic factors. This review seeks to compare the influence of genetic and non-genetic factors on the association between serotonin and suicide risk. Examining serotonin-related gene polymorphisms, with a focus on the serotonin transporter gene, the serotonin receptor 1A, and the serotonin receptor 2A, genetic contributions are investigated. This review emphasizes the complex interplay between genetic and non-genetic contributions to serotonin’s role in suicide by synthesizing existing literature. Understanding these complex interactions can provide a comprehensive framework for targeted interventions and individualized methods of suicide prevention and mental health promotion. Future research should incorporate large-scale genetic studies, genetic and non-genetic interaction analyses, and longitudinal designs in order to further elucidate the complex relationship between serotonin and suicide risk.

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6

Szasz, Robert, and George L. Dale. "Thrombospondin and fibrinogen bind serotonin-derivatized proteins on COAT-platelets." Blood 100, no. 8 (October 15, 2002): 2827–31. http://dx.doi.org/10.1182/blood-2002-02-0354.

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Activation of platelets with 2 agonists, collagen and thrombin, reveals a subpopulation of cells referred to as COAT-platelets (collagen and thrombin activated). These cells are enriched in several membrane-bound, procoagulant proteins, including fibrinogen, thrombospondin, factor V, von Willebrand factor, and fibronectin. α-Granule proteins bound to COAT-platelets are derivatized with serotonin by a transglutaminase-mediated process, and the interaction of conjugated serotonins with unidentified serotonin binding sites on the platelet surface enhances retention of these proteins. We now demonstrate that both thrombospondin and fibrinogen provide the requisite serotonin binding sites. Thrombospondin and fibrinogen were identified using photoreactive cross-linking to an albumin-(serotonin)6conjugate during COAT-platelet production. We subsequently verified that biotin-albumin-(serotonin)6 binds in vitro to thrombospondin, fibrinogen, and fibrinogen fragment D in a saturable manner. These data support a model for COAT-platelets where serotonin-derivatized procoagulant proteins interact with their respective receptors (eg, fibrinogen with glycoprotein IIb/IIIa or factor V with phosphatidylserine) as well as serotonin binding sites on fibrinogen and thrombospondin, resulting in a stable, multivalent complex on the cell surface.

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7

Liu, Zhixiang, Rui Lin, and Minmin Luo. "Reward Contributions to Serotonergic Functions." Annual Review of Neuroscience 43, no. 1 (July 8, 2020): 141–62. http://dx.doi.org/10.1146/annurev-neuro-093019-112252.

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The brain serotonin systems participate in numerous aspects of reward processing, although it remains elusive how exactly serotonin signals regulate neural computation and reward-related behavior. The application of optogenetics and imaging techniques during the last decade has provided many insights. Here, we review recent progress on the organization and physiology of the dorsal raphe serotonin neurons and the relationships between their activity and behavioral functions in the context of reward processing. We also discuss several interesting theories on serotonin's function and how these theories may be reconciled by the possibility that serotonin, acting in synergy with coreleased glutamate, tracks and calculates the so-called beneficialness of the current state to guide an animal's behavior in dynamic environments.

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8

Matiș, Loredana, Lucia Georgeta Daina, Lavinia Maris, Timea Claudia Ghitea, Daniela Florina Trifan, Ioana Moga, and Radu Fodor. "Variety of Serotonin Levels in Pediatric Gastrointestinal Disorders." Diagnostics 13, no. 24 (December 15, 2023): 3675. http://dx.doi.org/10.3390/diagnostics13243675.

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(1) Serotonin primarily regulates our emotions. A complex process, which includes dysfunctions in gastrointestinal motility and deregulation of the gene responsible for serotonin reuptake (SERT), is implicated in the pathophysiology of irritable bowel syndrome (IBS). This also encompasses changes in intestinal microbiota, the response to stress, the intricate interplay between the brain and the digestive tract, heightened sensitivity to visceral stimuli, and low-grade inflammation. This paper aims to investigate the effectiveness of probiotic therapy in managing gastrointestinal and neuropsychiatric symptoms related to serotonin levels, with a focus on individuals with serotonin deficiency and those with normal serotonin levels experiencing gastrointestinal disorders. (2) The study involved 135 pediatric patients aged 5–18 years with gastrointestinal disturbances, including constipation, diarrhea, and other symptoms, such as nausea, flatulence, feeling full, or gastrointestinal pain. (3) Serotonin testing was performed, and administering probiotics appeared to be effective in addressing serotonin deficiency and other gastrointestinal disorders. (4) Serotonin’s pivotal role in regulating neurotransmitter secretion and its impact on neuropsychiatric health, coupled with gender differences and age-related declines, underscore the complexity of their influence on gastrointestinal and neuropsychiatric conditions.

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9

Von Ah, Diane, Todd Skaar, Fredrick Unverzagt, Menggang Yu, Jingwei Wu, Bryan Schneider, Anna Maria Storniolo, et al. "Evaluating the Role of Serotonin on Neuropsychological Function After Breast Cancer Using Acute Tryptophan Depletion." Biological Research For Nursing 14, no. 1 (December 30, 2010): 5–15. http://dx.doi.org/10.1177/1099800410393273.

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Although cognitive dysfunction is a prevalent and disruptive problem for many breast cancer survivors (BCSs), little research has examined its etiology. One potential mechanism that remains to be explored is serotonin. Serotonin has been implicated in normal and dysfunctional cognitive processes, and serotonin levels are significantly affected by estrogen withdrawal, a common side effect of breast cancer treatment. However, no study has evaluated serotonin’s role on cognitive dysfunction in BCSs. The purpose of this study was to examine the role of serotonin in cognitive dysfunction in survivors by lowering central serotonin concentrations via acute tryptophan depletion (ATD). Based on previous research in noncancer populations, we hypothesized that alterations in central serotonin levels would induce cognitive dysfunction in these women controlling for confounding characteristics such as fluctuating mood and glucose levels. Secondarily, we explored whether genetic variations in serotonin genes would partly explain ATD. Participants included 20 female BCSs, posttreatment for nonmetastatic breast cancer, who received ATD or control in a double-blind, crossover design. Cognitive performance was measured at the 5-hr tryptophan/serotonin nadir on each test day using standardized neuropsychological tests. Specific impairment was noted in episodic memory (delayed recall) and motor speed during ATD versus control. ATD did not alter new learning (immediate recall), working memory, verbal fluency, or information processing speed. Findings suggest that serotonin may play a critical role in memory consolidation and motor functioning in BCSs.

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10

Pascual, Julio. "Serotonin, serotonin receptors, serotonin receptor subtype agonists and pain." Pain 40, no. 1 (January 1990): 115–16. http://dx.doi.org/10.1016/0304-3959(90)91061-m.

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11

Garattini, Silvio, and Rosario Samanin. "Biochemical hypotheses on antidepressant drugs: a guide for clinicians or a toy for pharmacologists?" Psychological Medicine 18, no. 2 (May 1988): 287–304. http://dx.doi.org/10.1017/s0033291700007844.

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SynopsisThe development of knowledge about the mechanism of action of tricyclic and the so-called ‘atypical’ antidepressants (AD) is reviewed. The discovery of clinically active antidepressants with little or no effect on noradrenaline or serotonin uptake has disproved the widely accepted concept that inhibition of monoamine uptake is a prerequisite for antidepressant activity. Another serious objection to this hypothesis is that blockade of monoamine uptake occurs in a matter of minutes after administration while 2–3 weeks of repeated treatment are necessary for the clinical AD effect. Nevertheless, the effect of repeated treatment with AD is compatible with the hypothesis that changes in central monoamine transmission are involved in the clinical activity of these drugs. Major changes in monoamine function after repeated treatment with AD include: desensitization and reduced density of noradrenaline receptors coupled to the adenylcyclase system, opposite changes in the sensitivity of α1 (increased) and α2-adrenoreceptors (decreased), down regulation of serotonin2 receptors and complex changes in the behavioural and electrophysiological responsiveness to serotonin agonists, subsensitivity of presynaptic dopamine receptors and enhanced activity of the mesolimbic dopamine system, decreased and increased density of GABA-A and GABA-B receptors respectively and down regulation of [3H]benzodiazepine binding.It remains to be clarified whether some of these changes have larger roles than others or whether they all contribute to the AD activity. An important role of dopamine in the activity of AD drugs is suggested by findings in the forced swimming test, whereas both catecholamines seem to be involved in the attenuation of escape deficit provoked by inescapable shock (learned helplessness). No clear evidence for a role of serotonin (with the possible exception of serotonin1A receptors) or GABA has been obtained in these experimental models of depression. The general validity of these findings obviously rests on the assumption that these models represent significant aspects of human depression.

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12

Ken Gillman, P. "Triptans, Serotonin Agonists, and Serotonin Syndrome (Serotonin Toxicity): A Review." Headache: The Journal of Head and Face Pain 50, no. 2 (February 2010): 264–72. http://dx.doi.org/10.1111/j.1526-4610.2009.01575.x.

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13

Heiser, P., and H. Remschmidt. "Die selektiven Serotonin-Wiederaufnahmehemmer und die neueren Antidepressivasubstanzen in der Kinder- und Jugendpsychiatrie." Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie 30, no. 3 (August 2002): 173–83. http://dx.doi.org/10.1024//1422-4917.30.3.173.

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Zusammenfassung: Fragestellung: Seit der ersten Publikation über einen selektiven Serotonin-Wiederaufnahmehemmer (SSRI) 1974 kam es nicht nur zur Weiterentwicklung der Wirkstoffe aus der Gruppe der SSRI, sondern es sind auch neue Substanzgruppen entwickelt worden. Zu diesen neueren Substanzgruppen gehören, gegliedert nach dem pharmakologischen Wirkmechanismus, die Serotonin2-Antagonisten/Serotonin-Wiederaufnahmehemmer (SARI), die noradrenergen und selektiv serotonergen Antidepressiva (NaSSA), die Noradrenalin- und Dopamin-Wiederaufnahmehemmer (NDRI) und die Serotonin- und Noradrenalin-Wiederaufnahmehemmer (SNRI). In dieser Übersichtsarbeit werden die Wirkmechanismen und Nebenwirkungssprofile der neuen Antidepressivasubstanzen dargestellt und mit den älteren Substanzgruppen wie trizyklischen Antidepressiva (TZA), MAO-Hemmern (MAOH) und SSRI verglichen. Es werden Studien mit Antidepressiva bei Kindern und Jugendlichen mit Depression vorgestellt und verglichen, ob es Unterschiede zwischen den älteren und neueren Antidepressiva gibt. Methode: Es wurde eine Medline Recherche bis einschließlich Januar 2002 durchgeführt. Schlussfolgerungen: Die bis jetzt durchgeführten Studien mit den neueren Antidepressiva sind vielversprechend. Allerdings sind weitere doppelblind, Placebo-kontrollierte Studien notwendig.

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14

EISON, MICHAEL S. "Serotonin." Journal of Clinical Psychopharmacology 10, Supplement (June 1990): 26S—30S. http://dx.doi.org/10.1097/00004714-199006001-00006.

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15

Veasey, Sigrid Carlen. "Serotonin." American Journal of Respiratory and Critical Care Medicine 163, no. 5 (April 2001): 1045–47. http://dx.doi.org/10.1164/ajrccm.163.5.ed1101d.

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16

Hariri, Ahmad R., and Sarah M. Brown. "Serotonin." American Journal of Psychiatry 163, no. 1 (January 2006): 12. http://dx.doi.org/10.1176/appi.ajp.163.1.12.

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17

Dinan, T. G. "Serotonin." International Clinical Psychopharmacology 11 (March 1996): 19–22. http://dx.doi.org/10.1097/00004850-199603001-00004.

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18

Struder, H., J. M. Davis, R. R. Meeusen, and G. A. Hand. "SEROTONIN." Medicine & Science in Sports & Exercise 33, no. 5 (May 2001): S273. http://dx.doi.org/10.1097/00005768-200105001-01538.

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19

Fraer, Mony, and Fusun Kilic. "Serotonin." Hypertension 65, no. 5 (May 2015): 942–48. http://dx.doi.org/10.1161/hypertensionaha.114.05061.

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20

Ligneul, Romain, and Zachary F. Mainen. "Serotonin." Current Biology 33, no. 23 (December 2023): R1216—R1221. http://dx.doi.org/10.1016/j.cub.2023.09.068.

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21

SJOERDSMA, ALBERT, and MICHAEL G. PALFREYMAN. "History of Serotonin and Serotonin Disorders." Annals of the New York Academy of Sciences 600, no. 1 The Neurophar (October 1990): 1–8. http://dx.doi.org/10.1111/j.1749-6632.1990.tb16869.x.

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22

FULLER, RAY W., and DAVID T. WONG. "Serotonin Uptake and Serotonin Uptake Inhibition." Annals of the New York Academy of Sciences 600, no. 1 The Neurophar (October 1990): 68–80. http://dx.doi.org/10.1111/j.1749-6632.1990.tb16873.x.

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23

Samuels, Benjamin Adam, Indira Mendez-David, Charlène Faye, Sylvain André David, Kerri A. Pierz, Alain M. Gardier, René Hen, and Denis J. David. "Serotonin 1A and Serotonin 4 Receptors." Neuroscientist 22, no. 1 (December 8, 2014): 26–45. http://dx.doi.org/10.1177/1073858414561303.

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24

Gardner, David M., and Larry D. Lynd. "Sumatriptan Contraindications and the Serotonin Syndrome." Annals of Pharmacotherapy 32, no. 1 (January 1998): 33–38. http://dx.doi.org/10.1345/aph.17204.

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OBJECTIVE To determine the risk for serotonin syndrome associated with the concomitant use of sumatriptan and the currently contraindicated therapies, that is, the monoamine oxidase inhibitors (MAOIs), serotonin selective-reuptake inhibitors (SSRIs), and lithium. METHODOLOGY: A comprehensive search for reports of serotonin syndrome associated with sumatriptan use was conducted by using tertiary drug interaction literature, MEDLINE, EmBASE, Biological Abstracts, Current Contents, Reactions, ClinAlert, and the International Pharmaceutical Abstracts. In addition, related reports from the proprietary manufacturers, the Health Protection Branch of Health Canada, and the World Health Organization Collaborative Centre for International Drug Monitoring were also solicited. RESULTS The concurrent use of sumatriptan with an SSRI or lithium has been reported to cause symptoms suggestive of serotonin syndrome in 16 and 2 cases, respectively. There were no reports involving MAOIs. In general, the reports indicated a mild-to-moderate, self-limited course with some features consistent with the serotonin syndrome. We found published reports of sumatriptan use without adverse events involving 148 patients receiving SSRIs, 31 patients taking MAOIs, and a small number using lithium. CONCLUSIONS Clinical evidence supporting the strict contraindication of MAOIs, SSRIs, and lithium was not identified. The balance of documented clinical experience pertaining to the use of sumatriptan concurrently with SSRIs or lithium suggests that most patients tolerate this combination without incident. Because there is little reliable experience with sumatriptan in combination with MAOIs, we suggest that sumatriptan should continue to be avoided in patients taking these agents until further data demonstrating safety become available. OBJETIVO Determinar el riego de desarrollar el síndrome de la serotonina asociado al uso concomitante del sumatriptan con agentes inhibidores selectivos de la captura de la serotonina, inhibidores de la monoamina oxidasa (IMAO), y el litio. MÉTODOS Las fuentes de información incluyeron la literatura de interacciones medicamentosas, MEDLINE, EmBASE, Biological Abstracts, Current Contents, Reactions, ClinAlert, y International Pharmaceutical Abstracts. También reportes emanados por los fabricantes de estos medicamentos, la Rama de Protección de la Salud de Salud Canada, y el Centro Colaborativo de Monitoreo Internacional de Medicamentos de la Organización Mundial de la Salud. RESULTADOS Los resultados de la investigación sugieren la presencia del síndrome de la serotonina en 16 casos de pacientes que recibieron el sumatriptan con los inhibidores selectivos de la captura de la serotonina y en 2 casos de pacientes que recibieron el sumatriptan con el litio. No hubo reportes que involucrasen a los IMAO. Las manifestaciones clínicas de este síndrome están descritas en este artículo. En general, los reportes indican que el curso de este evento es de leve a moderado y auto limitante. Los autores consiguieron un número considerable de reportes de estas combinaciones que no condujeron a reacciones adversas. Estos incluyeron 148 reportes del uso del sumatriptan con inhibidores selectivos de la captura de la serotonina, 31 del uso del sumatriptan con IMAO, y un número pequeño del uso del sumatriptan con el litio. CONCLUSIONES No existe suficiente evidencia clínica de que los IMAO, los inhibidores selectivos de la captura de la serotonina o que el litio estén totalmente contraindicados en pacientes recibiendo el sumatriptan. La experiencia clínica documentada hasta el presente sugiere que la mayoría de los pacientes toleran esta combinación sin incidentes. Debido a que existe poca experiencia acerca del uso del sumatriptan con los IMAO, los autores sugieren que esta combinación sea evitada hasta que haya mayor información sobre su seguridad. OBJECTIF Préciser le risque d'apparition d'un syndrome sérotoninergique lié à l'emploi concomitant de sumatriptan et des inhibiteurs de la monoamine oxydase (IMAO), des inhibiteurs sélectifs de la recapture de la sérotonine (ISRS), ou du lithium. MÉTHODES Une recherche des rapports publiés sur le syndrome sérotoninergique lié à l'emploi du sumatriptan a été menée dans les sources d'informations spécialisées en interactions médicamenteuses, dans les banques informatisées MEDLINE et EmBASE, dans les revues Biological Abstracts, Current Contents, Reactions, ClinAlert, et International Pharmaceutical Abstracts. De plus, les données des fabricants, de la Direction Générale de la Protection de la Santé de Santé Canada, et du Centre de Collaboration pour la Surveillance Internationale des Médicaments de l'Organisation Mondiale de la Santé ont été révisées. RÉSULTATS L'emploi concomitant de sumatriptan et des ISRS ou du lithium a été associé à des symptômes s'apparentant au syndrome sérotoninergique dans 16 et 2 cas, respectivement. Il n'y a pas eu de cas rapporté avec les IMAO. En général, les symptômes rapportés étaient de légers à modérés, et quelques présentations concordaient avec un syndrome sérotoninergique. Les auteurs ont répertorié 148 patients ayant utilisé le sumatriptan et les ISRS qui n'ont eu aucun problème, 31 patients ayant eu des IMAO et quelquesuns ayant eu du lithium. CONCLUSIONS L'évidence clinique supportant une contre-indication absolue de l'emploi des IMAO, des ISRS, ou du lithium concomitamment à celle du sumatriptan n'a pu être démontrée. La plupart des patients tolèrent les associations sumatriptan et ISRS ou lithium sans incident. Comme il y a peu d'informations entourant l'utilisation concomitante du sumatriptan et des IMAO, les auteurs suggèrent qu'il serait prudent d'éviter cette association jusqu'à ce que des données supplémentaires montrent son inocuité.

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Akhmetova, М. Zh, R. R. Nigmatullina, F. А. Mindubayeva, and G. М. Tykezhanova. "Effect of serotonin on myocardial contractility in newborn rats with excess and deficiency of serotonin in the embryonic period." Bulletin of the Karaganda University. “Biology, medicine, geography Series” 101, no. 1 (March 29, 2021): 82–87. http://dx.doi.org/10.31489/2021bmg1/82-87.

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Serotonin as a neurotransmitter (5-HT) plays a crucial role in the cardiovascular system. Serotonin is a humoral system of regulators and modulators of physiological processes. Under pathological conditions, these processes can turn into factors contributing to the development of diseases such as atherosclerosis, arterial hypertension, and pulmonary hypertension. The 5-HT4 and 5-HT2B receptors are found in cardiomyocytes. During the embryonic period, serotonin acts as a growth factor and plays an important regulatory role in the crucial period of embryonic development, in particular, a heart of an embryo. Therefore, any interference with this system in the womb can disrupt the normal development of the cardiovascular system. In the given study, there is some data provided to indicate that a change in the serotonin concentration created by the serotonin synthesis and the membrane serotonin transporter blocked in the embryonic period of ontogenesis, affects the inotropic function of the right ventricular myocardium in early postnatal ontogenesis, which is caused by a change in the contraction time in the groups under the experiment. Thus, statistically the response of cardiomyocytes to serotonin is significantly higher in the group with an excess of serotonin and significantly lower in the group with a deficiency of serotonin compared to the control group.

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26

Kondoh, Mayumi, Takashi Shiga, and Nobuo Okado. "Regulation of dendrite formation of Purkinje cells by serotonin through serotonin1A and serotonin2A receptors in culture." Neuroscience Research 48, no. 1 (January 2004): 101–9. http://dx.doi.org/10.1016/j.neures.2003.10.001.

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27

Robertson, J. I. S. "Serotonin, serotonin antagonists, hypertension and vascular diseases." Current Opinion in Cardiology 3, no. 5 (September 1988): 702–14. http://dx.doi.org/10.1097/00001573-198809000-00007.

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Lane, Roger, and David Baldwin. "Selective Serotonin Reuptake Inhibitor-Induced Serotonin Syndrome." Journal of Clinical Psychopharmacology 17, no. 3 (June 1997): 208–21. http://dx.doi.org/10.1097/00004714-199706000-00012.

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Heath, Mark J. S., and René Hen. "Serotonin Receptors: Genetic insights into serotonin function." Current Biology 5, no. 9 (September 1995): 997–99. http://dx.doi.org/10.1016/s0960-9822(95)00199-0.

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Lee, H. J., M. K. Park, S. Y. Kim, H. Y. Park Choo, A. Y. Lee, and C. H. Lee. "Serotonin induces melanogenesis via serotonin receptor 2A." British Journal of Dermatology 165, no. 6 (October 17, 2011): 1344–48. http://dx.doi.org/10.1111/j.1365-2133.2011.10490.x.

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Dean, Brian, Wendy Hayes, Kenneth Opeskin, Lee Naylor, Geoffrey Pavey, Christine Hill, Nicholas Keks, and David L. Copolov. "Serotonin2 receptors and the serotonin transporter in the schizophrenic brain." Behavioural Brain Research 73, no. 1-2 (December 1995): 169–75. http://dx.doi.org/10.1016/0166-4328(96)00091-5.

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Sizemore, Tyler R., Laura M. Hurley, and Andrew M. Dacks. "Serotonergic modulation across sensory modalities." Journal of Neurophysiology 123, no. 6 (June 1, 2020): 2406–25. http://dx.doi.org/10.1152/jn.00034.2020.

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The serotonergic system has been widely studied across animal taxa and different functional networks. This modulatory system is therefore well positioned to compare the consequences of neuromodulation for sensory processing across species and modalities at multiple levels of sensory organization. Serotonergic neurons that innervate sensory networks often bidirectionally exchange information with these networks but also receive input representative of motor events or motivational state. This convergence of information supports serotonin’s capacity for contextualizing sensory information according to the animal’s physiological state and external events. At the level of sensory circuitry, serotonin can have variable effects due to differential projections across specific sensory subregions, as well as differential serotonin receptor type expression within those subregions. Functionally, this infrastructure may gate or filter sensory inputs to emphasize specific stimulus features or select among different streams of information. The near-ubiquitous presence of serotonin and other neuromodulators within sensory regions, coupled with their strong effects on stimulus representation, suggests that these signaling pathways should be considered integral components of sensory systems.

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James, Arlene N., James P. Ryan, Michael D. Crowell, and Henry P. Parkman. "Regional gastric contractility alterations in a diabetic gastroparesis mouse model: effects of cholinergic and serotoninergic stimulation." American Journal of Physiology-Gastrointestinal and Liver Physiology 287, no. 3 (September 2004): G612—G619. http://dx.doi.org/10.1152/ajpgi.00431.2003.

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The C57BLKS/J db/ db mouse develops hyperglycemia and has delayed gastric emptying that is improved with tegaserod, a partial 5-HT4 agonist. Our aims here were to determine regional gastric contractility alterations in C57BLKS/J db/ db mice and to determine the effects of serotonin and tegaserod. The contractile effects of bethanechol, serotonin, and tegaserod in fundic, antral, and pyloric circular muscle were compared in C57BLKS/J db/ db mice and normal littermates. The effects of tetrodotoxin, atropine, and 5-HT receptor antagonists were studied. Contractions in response to bethanechol were decreased in the fundus, similar in the antrum, but increased in the pylorus in diabetic mice compared with controls. Serotonin and, to a lesser extent, tegaserod caused contractions that were more pronounced in the fundus than in the antrum and pylorus in both diabetic and normal mice. Serotonin-induced contractions were partially inhibited by atropine, the 5-HT4 antagonist GR113808, and the 5-HT2 antagonist cinanseron but not tetrodotoxin. Regional gastric contractility alterations are present in this diabetic gastroparesis mouse model. Fundic contractility was decreased, but pyloric contractility was increased in the pylorus to cholinergic stimulation in diabetic mice. Serotonin's contractile effect is mediated, in part, through muscarinic, 5-HT2, and 5-HT4 receptors. This study suggests that fundic hypomotility and pyloric hypercontractility, rather than antral hypomotility, play important roles for the gastric dysmotility that occurs in diabetes.

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Rizal, Raisha Rahmani, and Dewi Nur Fiana. "Sindrom Serotonin." Medical Profession Journal of Lampung 11, no. 2 (July 31, 2019): 174–82. http://dx.doi.org/10.53089/medula.v11i2.186.

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Sindrom serotonin (SS) (juga disebut sebagai toksisitas serotonin) adalah toksidrom yang diinduksi obat yang berpotensi mengancam jiwa yang terkait dengan peningkatan aktivitas serotonergik di sistem saraf perifer (PNS) dan pusat (SSP). Hal ini ditandai dengan spektrum yang relevan dengan dosis dari temuan klinis yang terkait dengan tingkat serotonin bebas (5-hydroxytryptamine [5-HT]), atau aktivasi reseptor 5-HT (terutama subtipe 5-HT1A dan 5-HT2A), yang mana termasuk kelainan neuromuskuler, hiperaktif otonom, dan perubahan keadaan mental. Meskipun sindrom serotonin jarang menyebabkan kematian, kasus yang parah adalah keadaan darurat medis yang dapat dengan cepat menyebabkan kegagalan organ multisistem Meskipun banyak obat telah terlibat dalam Sindrom serotonin, kasus yang mengancam jiwa umumnya terjadi hanya ketika inhibitor oksidase monoamine dikombinasikan dengan penghambat serotonin re-uptake selektif atau nonselektif. Kesadaran tentang Sindrom serotonin sangat penting tidak hanya dalam menghindari kombinasi obat-obatan terapeutik yang berbahaya yang tidak disengaja tetapi juga dalam mengenali gambaran klinis ketika terjadi sehingga pengobatan dapat segera dimulai. Dalam ulasan ini, patofisiologi, gambaran klinis, obat yang terlibat dan diagnosis Sindrom serotonin dibahas.

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Comet, Marie-Anne, Caroline Sévoz-Couche, Naïma Hanoun, Michel Hamon, and Raul Laguzzi. "5-HT-mediated inhibition of cardiovagal baroreceptor reflex response during defense reaction in the rat." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 4 (October 2004): H1641—H1649. http://dx.doi.org/10.1152/ajpheart.01204.2003.

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Previous studies showed that the cardiac response of the baroreceptor reflex (bradycardia) is inhibited during the defense reaction evoked by direct electrical or chemical stimulation of the periaqueductal gray (dPAG) in the rat. Whether central serotonin and nucleus tractus solitarius (NTS) serotonin3 (5-HT3) receptors might participate in this inhibition was investigated in urethane-anesthetized and atenolol-pretreated rats. Our results showed that both electrical and chemical stimulation of the dPAG produced a drastic reduction of the cardiovagal component of the baroreceptor reflex triggered by either intravenous administration of phenylephrine or aortic nerve stimulation. This inhibitory effect of dPAG stimulation on the baroreflex bradycardia was not observed in rats that had been pretreated with p-chlorophenylalanine (300 mg/kg ip daily for 3 days) to inhibit serotonin synthesis. Subsequent 5-hydroxytryptophan administration (60 mg/kg ip), which was used to restore serotonin synthesis, allowed the inhibitory effect of dPAG stimulation on both aortic and phenylephrine-induced cardiac reflex responses to be recovered in p-chlorophenylalanine-pretreated rats. On the other hand, in nonpretreated rats, the inhibitory effect of dPAG stimulation on the cardiac baroreflex response could be markedly reduced by prior intra-NTS microinjection of granisetron, a 5-HT3 receptor antagonist, or bicuculline, a GABAA receptor antagonist. These results show that serotonin plays a key role in the dPAG stimulation-induced inhibition of the cardiovagal baroreceptor reflex response. Moreover, they support the idea that 5-HT3 and GABAA receptors in the NTS contribute downstream to the inhibition of the baroreflex response caused by dPAG stimulation.

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Kema, I. P., E. G. de Vries, A. M. Schellings, P. E. Postmus, and F. A. Muskiet. "Improved Diagnosis of Carcinoid Tumors by Measurement of Platelet Serotonin." Clinical Chemistry 38, no. 4 (April 1, 1992): 534–40. http://dx.doi.org/10.1093/clinchem/38.4.534.

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Abstract Carcinoid patients are diagnosed biochemically on the basis of increased urinary excretion of 5-hydroxyindoleacetic acid (5-HIAA); urinary and platelet serotonin concentrations are considered to provide complementary information. Using established HPLC methods with fluorometric detection, we evaluated the clinical usefulness of measurements of urinary 5-HIAA and urinary, plasma, and platelet serotonin in 30 consecutive patients with histologically proven carcinoid tumors of fore-, mid-, and hindgut origin before treatment. Ten patients showed no signs of serotonin overproduction; 14 had increased concentrations of urinary 5-HIAA and platelet serotonin; and platelet serotonin, but not urinary 5-HIAA, was increased in 6. None had increased urinary 5-HIAA excretion without an increase in platelet serotonin content. In cases with high rates of tumor serotonin secretion, platelet serotonin reached a maximum and did not correlate with serotonin secretion rate, whereas urinary 5-HIAA was correlated. Increased platelet serotonin was correlated with increased plasma serotonin and with occurrence of carcinoid syndrome. Increased urinary serotonin, allegedly caused by increases in circulating 5-hydroxytryptophan, almost invariably coincided with increased platelet serotonin, but not necessarily with above-normal urinary 5-HIAA excretion. From these results and long-term monitoring of three patients during treatment, we conclude that platelet serotonin is more sensitive than urinary 5-HIAA for detecting carcinoids that secrete only small amounts of serotonin.

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Matondo, Ramadhan B., Carine Punt, Judith Homberg, Mathilda J. M. Toussaint, Ronald Kisjes, Suzanne J. A. Korporaal, Jan Willem N. Akkerman, Edwin Cuppen, and Alain de Bruin. "Deletion of the serotonin transporter in rats disturbs serotonin homeostasis without impairing liver regeneration." American Journal of Physiology-Gastrointestinal and Liver Physiology 296, no. 4 (April 2009): G963—G968. http://dx.doi.org/10.1152/ajpgi.90709.2008.

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The serotonin transporter is implicated in the uptake of the vasoconstrictor serotonin from the circulation into the platelets, where 95% of all blood serotonin is stored and released in response to vascular injury. In vivo studies indicated that platelet-derived serotonin mediates liver regeneration after partial hepatectomy. We have recently generated serotonin transporter knockout rats and demonstrated that their platelets were almost completely depleted of serotonin. Here we show that these rats exhibit impaired hemostasis and contain about 1–6% of wild-type serotonin levels in the blood. Despite the marked reduction of serotonin levels in blood and platelets, efficient liver regeneration and collagen-induced platelet aggregation occur in rats lacking the serotonin transporter. These results provide evidence that liver regeneration is not dependent on the release of serotonin from platelets. Our findings indicate that very low levels of serotonin in blood are sufficient for liver regeneration.

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Bartlett, Dana. "Drug-Induced Serotonin Syndrome." Critical Care Nurse 37, no. 1 (February 1, 2017): 49–54. http://dx.doi.org/10.4037/ccn2017169.

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Serotonin syndrome is a potentially fatal condition caused by drugs that affect serotonin metabolism or act as serotonin receptor agonists. Monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, and serotonin-norepinephrine reuptake inhibitors are the medications most commonly associated with serotonin syndrome. Serotonin syndrome can be mild and of short duration, but a prolonged course, life-threatening complications, and death are possible. Detection of serotonin syndrome is not difficult if the diagnostic criteria are understood and properly used, but the syndrome has no confirmatory tests and other drug-induced syndromes can, to a degree, mimic serotonin syndrome. The treatment is symptomatic and supportive. Antidotal therapies are available, but the evidence for their effectiveness is limited. If serotonin syndrome is promptly identified and aggressively treated, the patient should fully recover.

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39

Hall, Michael, and Nick Buckley. "Serotonin syndrome." Australian Prescriber 26, no. 3 (June 1, 2003): 62–63. http://dx.doi.org/10.18773/austprescr.2003.044.

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Gillman, Ken, Felicity Prior, M. Hall, and N. Buckley. "Serotonin syndrome." Australian Prescriber 26, no. 5 (October 1, 2003): 99–102. http://dx.doi.org/10.18773/austprescr.2003.074.

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41

Bulut, Utku. "Serotonin syndrome." Journal of Parkinson’s Disease and Movement Disorders 22, no. 1-2 (March 16, 2020): 33–38. http://dx.doi.org/10.5606/phhb.dergisi.2019.006.

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Stahl, Stephen M. "Serotonin Receptors." Psychiatric Annals 26, no. 8 (August 1, 1996): 505–7. http://dx.doi.org/10.3928/0048-5713-19960801-03.

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&NA;. "Serotonin modulators." Reactions Weekly &NA;, no. 903 (May 2002): 11. http://dx.doi.org/10.2165/00128415-200209030-00039.

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Lejoyeux, Michel, Jean Adès, and Frédéric Rouillon. "Serotonin Syndrome." CNS Drugs 2, no. 2 (August 1994): 132–43. http://dx.doi.org/10.2165/00023210-199402020-00006.

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Westphal, R. J. "Serotonin Syndrome." Journal of the American Psychiatric Nurses Association 5, no. 3 (June 1999): 97–102. http://dx.doi.org/10.1177/107839039900500304.

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Takeshi Inoue, Bentham Science Publisher, Bentham Science Publisher Ichiro Kusumi, and Bentham Science Publisher Mitsuhiro Yoshioka. "Serotonin Transporters." Current Drug Target -CNS & Neurological Disorders 1, no. 5 (October 1, 2002): 519–29. http://dx.doi.org/10.2174/1568007023338987.

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Buckley, N. A., A. H. Dawson, and G. K. Isbister. "Serotonin syndrome." BMJ 348, feb19 6 (February 19, 2014): g1626. http://dx.doi.org/10.1136/bmj.g1626.

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Van Kempen, G. M. "Plasma serotonin." Journal of Neurology, Neurosurgery & Psychiatry 53, no. 9 (September 1, 1990): 819–20. http://dx.doi.org/10.1136/jnnp.53.9.819-c.

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Bodner, R. A., T. Lynch, L. Lewis, and D. Kahn. "Serotonin syndrome." Neurology 45, no. 2 (February 1, 1995): 219–23. http://dx.doi.org/10.1212/wnl.45.2.219.

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Gevirtz, Clifford. "Serotonin Syndrome." Topics in Pain Management 22, no. 3 (October 2006): 1–6. http://dx.doi.org/10.1097/00587875-200610000-00001.

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