Gotowe bibliografie tematyczne / Serotonin

Gotowa bibliografia na temat „Serotonin”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 30 lipca 2024

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Artykuły w czasopismach na temat "Serotonin"

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Park, K. H., J. P. Long i J. G. Cannon. "Effects of serotonin1-like receptor agonists on autonomic neurotransmission". Canadian Journal of Physiology and Pharmacology 69, nr 12 (1.12.1991): 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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Lippton, H. L., Q. Hao i A. Hyman. "L-NAME enhances pulmonary vasoconstriction without inhibiting EDRF-dependent vasodilation". Journal of Applied Physiology 73, nr 6 (1.12.1992): 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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Balakrishna, Pragathi, Sagila George, Hassan Hatoum i Sarbajit Mukherjee. "Serotonin Pathway in Cancer". International Journal of Molecular Sciences 22, nr 3 (28.01.2021): 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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Sarkar, Parijat, Kaleeckal G. Harikumar, Satinder S. Rawat, Sanjib Das, Tushar K. Chakraborty i Amitabha Chattopadhyay. "Environment-Sensitive Fluorescence of 7-Nitrobenz-2-oxa-1,3-diazol-4-yl (NBD)-Labeled Ligands for Serotonin Receptors". Molecules 26, nr 13 (24.06.2021): 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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Lee, Jeon Lo. "A Comparison of Genetic versus Non-Genetic Contribution of Serotonin to Suicide". Science Insights 43, nr 1 (31.07.2023): 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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Szasz, Robert, i George L. Dale. "Thrombospondin and fibrinogen bind serotonin-derivatized proteins on COAT-platelets". Blood 100, nr 8 (15.10.2002): 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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Liu, Zhixiang, Rui Lin i Minmin Luo. "Reward Contributions to Serotonergic Functions". Annual Review of Neuroscience 43, nr 1 (8.07.2020): 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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Matiș, Loredana, Lucia Georgeta Daina, Lavinia Maris, Timea Claudia Ghitea, Daniela Florina Trifan, Ioana Moga i Radu Fodor. "Variety of Serotonin Levels in Pediatric Gastrointestinal Disorders". Diagnostics 13, nr 24 (15.12.2023): 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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Von Ah, Diane, Todd Skaar, Fredrick Unverzagt, Menggang Yu, Jingwei Wu, Bryan Schneider, Anna Maria Storniolo i in. "Evaluating the Role of Serotonin on Neuropsychological Function After Breast Cancer Using Acute Tryptophan Depletion". Biological Research For Nursing 14, nr 1 (30.12.2010): 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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Pascual, Julio. "Serotonin, serotonin receptors, serotonin receptor subtype agonists and pain". Pain 40, nr 1 (styczeń 1990): 115–16. http://dx.doi.org/10.1016/0304-3959(90)91061-m.

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Rozprawy doktorskie na temat "Serotonin"

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Edgar, Christopher James. "Serotonin and attention". Thesis, Northumbria University, 2007. http://nrl.northumbria.ac.uk/2896/.

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The serotonergic system along with other brain neurotransmitter systems has been implicated in the modulation of cognitive function. Dysregulation or pathology in neurotransmitter systems is thought to underlie the cognitive impairments associated with normal ageing, a number of disease states and chronic drug abuse. Research into the influence of serotonergic systems on cognition has focussed on the modulation of other neurotransmitter systems by serotonergic input and the importance of serotonergic receptor subtypes for learning and memory. There is evidence supporting an action of serotonin to inhibit attentional processes, perhaps primarily through inhibition of dopaminergic function, but also via other neurotransmitter systems critical to attentional function such as the noradrenergic and cholinergic systems. Studies indicate that the serotonin selective reuptake inhibitors may impair aspects of attention, whilst acute tryptophan depletion to reduce serotonin synthesis and release, may enhance aspects of attention. These data have resulted in several researchers proposing general theories of serotonergic inhibition, particularly in respect to attention/arousal. However, differential effects may be seen from studies of the various serotonergic receptor subtypes, which have so far been targeted, indicating a general theory may not be sufficient to explain the data. The evidence presented in this thesis demonstrates that some of the paradigms used thus far to support general theories of serotonergic inhibition of attention/arousal may be flawed. Specifically, monoamine depletion studies may not be able to separate serotonergic and dopaminergic influences on cognition, whilst studies of selective serotonin reuptake inhibitors and chronic ecstasy use have not controlled well for influences of sleep on cognition. Furthermore, evidence from studies of the serotonin receptor subtypes may indicate effects specific to neuropsychological processes underlying measures of attention/arousal or differential effects on aspects of cognition, which may contradict a general theory of inhibition. In conclusion, general theories of inhibition are still sufficient to account for the majority of data. However, in further academic and clinical research, thorough investigation of cognition will be critical to the development of more detailed theory and the development of effective drug treatments for cognitive disorders. Furthermore, the consideration of confounding factors in research such as the influence of sleep on cognition and the competition between monoamines for transport, is critical to the understanding and interpretation of the scientific literature to date.
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Wang, Chung-Chi. "Regulation of hepatic glucose metabolism by serotonin and serotonin receptor agonists". Thesis, University of Newcastle Upon Tyne, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.578261.

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The transition from net glucose production by the liver to net glucose uptake after a meal is regulated by glucose, insulin and glucagon and by neurotransmitters via mechanisms that are as yet uncharacterised. This study investigated the direct effects of serotonin on glucose metabolism in freshly isolated hepatocytes. Serotonin (5-hydroxytryptamine, 5-HT) is both a neurotransmitter and a hormone produced by the gut in the postprandial state that exerts its target actions through multiple families of 5-HT receptors (5-HTl-7). 5-HT caused a concentration-dependent stimulation of glycogen synthesis in hepatocytes maintained in short-term culture that was counteracted by antagonists of 5-HTl receptors and enhanced by antagonists of 5-HT2BC receptors. Selective agonists of 5-HTl receptors (5-HTIA, 5-HTIB and 5-HTIF), m-5-HT and 5-HT2 receptors provided evidence for a stimulatory pathway mediated by 5-HTl receptors and an inhibitory pathway mediated by 5-HT2 receptors. The activation of the stimulatory pathway was counteracted by the antipsychotic drug olanzapine. M-5-HT (a-Methyl 5-hydroxytryptamine) and selective agonists for 5-HTl receptors were used to study the stimulatory signalling pathway. The stimulation of glycogen synthesis by m-5-HT (and 5-HTl receptor agonists) was greater than the stimulation induced by insulin and was associated with inactivation of glycogen phosphorylase (conversion of phosphorylase-a to phosphorylase-b) and activation of glycogen synthase without stimulation of glucose phosphorylation or glycolysis. M-5-HT counteracted the activation of glycogen phosphorylase caused by forskolin and dibutyryl-cAMP but it did not counteract the inhibition of glycolysis or the phosphorylation of the protein kinase A (PKA) substrate phosphofructokinase-2/fructose bisphosphatase-2 (Ser32) suggesting a selective effect on the glycogenic pathway as opposed to a signalling pathway upstream of PKA. Unlike insulin action the glycogenic stimulation by m-5-HT was not blocked by wortmannin, a PI 3-kinase inhibitor, and it was not associated with activation of PKB. However, it was partially counteracted by inhibitors of cdk5 including roscovitine, kenpaullone and purvanalol. Overexpression of cdk5 and its eo-regulator p35 mimicked the stimulation of glycogen synthesis by m-5-HT supporting a role for cdk5 in control of glycogen synthesis. M-5-HT caused increased phosphorylation of both protein phosphatase-l (Thr320) and its regulatory protein, inhibitor-2 (Thr72), which are substrates of cdk5. This supports a possible role for cdk5 in the glycogenic stimulation bym-5-HT. This study provides evidence that agonists of 5-HTl receptors stimulate hepatic glycogen synthesis by a novel signalling pathway that is totally distinct from the insulin signalling pathway and involves inactivation of glycogen phosphorylase and possibly activation of cdk5. The counteraction of this pathway by olanzapine provides a possible explanation for the impaired glucose tolerance caused by this currently used drug. 11
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Lecours, Maurice. "Electrophysiological Investigations on the Role of Selected Serotonin Receptors and the Serotonin Transporter on Serotonin Transmission in the Rat Brain". Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/30400.

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This study assessed the in vivo effects of various serotonin (5-HT) receptor modulators on 5-HT neurotransmission in the rat hippocampus. Vortioxetine, humanized-vortioxetine, and escitalopram blocked the 5-HT transporter, but similar to ipsapirone did not dampen the sensitivity of postsynaptic 5-HT1A receptors. Long-term administration of all treatments increased the tonic activation of postsynaptic 5-HT1A heteroreceptors, an effect common to all antidepressants. Vortioxetine decreased the function of the terminal 5-HT1B autoreceptor under high but not a low degree of activation, thus showing that its partial agonism led to increased 5-HT release and that long-term administration results in the desensitization of terminal 5-HT1B autoreceptors. Vortioxetine overcame the effects of 5-HT1B and 5-HT3 receptor agonists. This study was unable to determine the involvement of 5-HT7 receptor antagonism exerted by vortioxetine affects 5-HT neurotransmission. Therefore, vortioxetine would appear to exert different actions, via transporter and receptor activity, on the serotonergic system in the hippocampus, consistent with its unique pharmacological profile.
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Parrish, Leslie. "Love and Low Serotonin". TopSCHOLAR®, 2008. http://digitalcommons.wku.edu/theses/371.

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The following is a novella that depicts a young man and woman in search of differing goals, but the essence of their goals does have something in common: each of their pursuits, if obtained, allows for self-control and recovered lifestyle. However, their lives are far from average throughout the story. Themes such as bulimia, drug use, loveless sex, voyeurism, lucid dreaming and emergency room healthcare are explored in the form of fiction. Both of the main characters in this story explore their world with a measure of obsession, and like any worthy character, their obsessions transform into decisions and actions that highlight aspects of society and psychology; in this case it is American college culture and youthful minds. It is up to the reader to become an explorer also. S/he may turn the pages with an objective mind, or with a sympathetic one. Either will be presented with the same questions: questions concerning self-image, companionship, healthcare socioeconomics, and deviant behavior.
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Selvaraj, Sudhaker. "Serotonin transporters in depression". Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.540258.

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Heath, D. G. "Triazolopyridines as serotonin analogues". Thesis, Imperial College London, 1985. http://hdl.handle.net/10044/1/37721.

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Porter, Richard J. "Corticosteroid serotonin interactions in depression". Thesis, University of Newcastle upon Tyne, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289200.

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Stuart, E. "Biochemical studies on serotonin receptors". Thesis, University of Nottingham, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.372014.

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Schaechter, Judith Diane. "Tryptophan availability modulates serotonin release". Thesis, Massachusetts Institute of Technology, 1989. http://hdl.handle.net/1721.1/13995.

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Gustafson, Megan Alyse. "Serotonin signaling in C. elegans". Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/40957.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2007.
Includes bibliographical references.
Wild-type animals that have been acutely food deprived slow their locomotory rate upon encountering bacteria more than do well-fed animals. This behavior, called the enhanced slowing response, is partly serotonin (5-HT) dependent. Animals mutant for the 5-HT reuptake transporter gene mod-5 slow even more than wild-type animals because endogenous 5-HT activity is potentiated. This behavior, called the hyperenhanced slowing response, can be suppressed by mutations in genes that encode proteins important for 5-HT signaling, like the 5-HT receptor encoded by mod-1 and the Ga subunit of a G protein encoded by goa-1. This ability to suppress indicates that these genes likely act downstream of or in parallel to one or more 5-HT synapse(s) that mediate(s) the enhanced slowing response. To find genes that play a role in 5-HT signaling, we screened for suppressors of the 5-HT hypersensitivity of mod-5. We found at least seven alleles of goa-i and at least two alleles of mod-1. This shows that our screen is able to target genes that play a role in endogenous 5-HT signaling. We identified two alleles of the FMRFamide-encoding gene fp-1, which was known to mediate paralysis in exogenous 5-HT. We showed that loss-of-function mutations in flp-1 confer an enhanced slowing response defect. We also identified an allele of abts-1, which encodes a bicarbonate transporter, and showed that it has defects in cholinergic signaling. We identified three mutants that show linkage to LG I, four to II, three to V and one to X, most of which display defects consistent with a role in 5-HT signaling.
(cont.) We used a candidate gene approach to find that deletions in ser-4, which encodes a metabotropic 5-HT receptor, confer 5-HT resistance. ser-4 acts redundantly with the ionotropic 5-HT receptor mod-1 to suppress the hyperenhanced slowing response of mod-5. Our genetic analysis suggests that ser-4 acts in a pathway with goa-1, in parallel to mod-1. We found that the enhanced slowing response defect of flp-1 is primarily due to its defect in transmitting a 5-HT signal and that flp-1 likely acts downstream of ser-4 and mod-1.
by Megan Alyse Gustafson.
Ph.D.
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Książki na temat "Serotonin"

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Vanhoutte, P. M., P. R. Saxena, R. Paoletti, N. Brunello i A. S. Jackson, red. Serotonin. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1920-7.

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Paoletti, Rodolfo, Paul M. Vanhoutte, Nicoletta Brunello i Franco M. Maggi, red. Serotonin. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1912-9.

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Mylecharane, Ewan J., James A. Angus, Ivan S. de la Lande i Patrick P. A. Humphrey, red. Serotonin. London: Palgrave Macmillan UK, 1989. http://dx.doi.org/10.1007/978-1-349-10114-6.

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N, Osborne Neville, i Hamon Michel, red. Neuronal serotonin. Chichester [West Sussex]: Wiley, 1988.

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Sanders-Bush, Elaine, red. The Serotonin Receptors. Totowa, NJ: Humana Press, 1988. http://dx.doi.org/10.1007/978-1-4612-4560-5.

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Roth, Bryan L., red. The Serotonin Receptors. Totowa, NJ: Humana Press, 2006. http://dx.doi.org/10.1007/978-1-59745-080-5.

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Blenau, Wolfgang, i Arnd Baumann, red. Serotonin Receptor Technologies. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2187-4.

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Maximino, Caio. Serotonin and Anxiety. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4048-2.

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Wurtman, Judith J. The Serotonin solution. New York: Fawcett Columbine, 1997.

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Elaine, Sanders-Bush, red. The Serotonin receptors. Clifton, N.J: Humana Press, 1988.

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Części książek na temat "Serotonin"

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Nueten, J. M. Van, P. A. J. Janssen, W. J. Janssens i P. M. Vanhoutte. "The Development of 5-HT2 Receptor Antagonists". W Serotonin, 3–11. London: Palgrave Macmillan UK, 1989. http://dx.doi.org/10.1007/978-1-349-10114-6_1.

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de la Lande, I. S., i E. J. Mylecharane. "Neuronal Actions of 5-Hydroxytryptamine: An Overview". W Serotonin, 77–83. London: Palgrave Macmillan UK, 1989. http://dx.doi.org/10.1007/978-1-349-10114-6_10.

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Tricklebank, M. D. "Behavioural Correlates of the Activation of 5-HT Receptors". W Serotonin, 87–94. London: Palgrave Macmillan UK, 1989. http://dx.doi.org/10.1007/978-1-349-10114-6_11.

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Tyers, M. B., B. Costall i R. J. Naylor. "5-HT3 Receptors in the Central Nervous System". W Serotonin, 95–100. London: Palgrave Macmillan UK, 1989. http://dx.doi.org/10.1007/978-1-349-10114-6_12.

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Bevan, P., B. Olivier, J. Schipper i J. Mos. "Serotoninergic Function and Aggression in Animals". W Serotonin, 101–8. London: Palgrave Macmillan UK, 1989. http://dx.doi.org/10.1007/978-1-349-10114-6_13.

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Langer, S. Z. "Behavioural Actions of 5-Hydroxytryptamine: An Overview". W Serotonin, 109–12. London: Palgrave Macmillan UK, 1989. http://dx.doi.org/10.1007/978-1-349-10114-6_14.

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Saxena, P. R. "Cardiac Actions of 5-Hydroxytryptamine". W Serotonin, 115–22. London: Palgrave Macmillan UK, 1989. http://dx.doi.org/10.1007/978-1-349-10114-6_15.

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de la Lande, I. S., J. A. Kennedy i B. J. Stanton. "Amplifying Action of 5-Hydroxytryptamine in the Rabbit Ear Artery". W Serotonin, 123–29. London: Palgrave Macmillan UK, 1989. http://dx.doi.org/10.1007/978-1-349-10114-6_16.

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Purdy, R. E., i D. L. Murray. "Serotonin-induced Vasoconstriction and Contractile Synergism with Noradrenaline: Role of α-Adrenoceptors". W Serotonin, 130–35. London: Palgrave Macmillan UK, 1989. http://dx.doi.org/10.1007/978-1-349-10114-6_17.

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Mylecharane, E. J., i C. A. Phillips. "Pre-synaptic Sympathetic Inhibition and 5-Hydroxytryptamine-induced Vasodilatation". W Serotonin, 136–45. London: Palgrave Macmillan UK, 1989. http://dx.doi.org/10.1007/978-1-349-10114-6_18.

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Streszczenia konferencji na temat "Serotonin"

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Seisdedos, R., i P. Lopez. "5PSQ-034 Linezolid and serotonin syndrome". W 24th EAHP Congress, 27th–29th March 2019, Barcelona, Spain. British Medical Journal Publishing Group, 2019. http://dx.doi.org/10.1136/ejhpharm-2019-eahpconf.467.

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Rosemann, Eric, i Peter Korian. "Exploring Serotonin in the GI Tract". W ACM SIGGRAPH 2001 video review. New York, New York, USA: ACM Press, 2001. http://dx.doi.org/10.1145/945191.945208.

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Alzghoul, B. N., A. A. Innabi, M. E. Langston, C. J. Patel, M. Chizinga, R. Reddy, H. M. Alnuaimat i A. Ataya. "Prevalence of Echocardiographic Pulmonary Hypertension in Patients Using Selective Serotonin and Selective Serotonin/Norepinephrine Reuptake Inhibitors". W American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3862.

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Morante, A., A. S. Khan i K. Oh. "Phencyclidine and Triple C Overdose Leading to Serotonin Syndrome in the Absence of Selective Serotonin Reuptake Inhibitors". W American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1672.

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DOLBERG, O. T., Y. SASSON, S. KINDLER, R. COHEN, M. KOTLER i J. ZOHAR. "SEROTONIN RECEPTOR SUBSETS IN OBSESSIVE-COMPULSIVE DISORDER". W IX World Congress of Psychiatry. WORLD SCIENTIFIC, 1994. http://dx.doi.org/10.1142/9789814440912_0023.

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Kaushalya, S. K., Suman Nag, J. Balaji i S. Maiti. "Serotonin: multiphoton imaging and relevant spectral data". W Biomedical Optics (BiOS) 2008, redaktorzy Ammasi Periasamy i Peter T. C. So. SPIE, 2008. http://dx.doi.org/10.1117/12.763020.

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Kanzaki, M., H. Kimura i J. Ochi. "IMMUNOHISTOCHEMICAL LOCALISATION OF SEROTONIN IN RABBIT PLATELETS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644884.

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Although it has been accepted that the dense bodymay be the most predominant storage site of serotonin (5HT), some literatures suggested that 5KT was localized more abundantly in the alpha-granules or theplasma membrane than in the dense body. The discrepancy may be due to different methods used.For example, the former dense body theory is mostly based on biochemical measurements of 5HT which may easily diffusible among subcellular fractions, and the latter hypothesis is proposed by autoradiographic demonstration of exogenously applied 5HT. In the present study, endogenous 5HT has been visualized by immunoelectron microscopy using monoclonal antibody against 5HT.Platelet rich plasma (PRP) of rabbits was suspended for 30 min in a fixative containing 0.5% glutaraldehyde, 4% paraformaldehyde and 0.5% picric acid in 0.1M phosphate buffer (PB; pH 7.4), and resuspended overnight in the glutaraldehyde-free fixative. After wash the PRP was incubated for 3 days with PB containing saline and 0.03% Triton X-100 (PBST), and reacted for 3 days with monoclonal 5HT antibody ( 1μg/ml). The immunoreactive sites were rendered visible byABC immunohistochemistry (ABC from Vector Co. USA) with DAB precipitation. The colorized PRP was osmificated (1%) for 30 min, dehydrated with alcohol, embedded in Spurr and cut into ultrathin sections for electron microscopic observation. For immunohistochemical controls monoclonal 5HT antibody preabsorbed with O.lmM 5HT or non-immune normal mouse serum was used as the primary antibody, and no specific reaction was observed. Very fine 5HT-positive immunoreaction products were clearly localized in some granules with different staining intensity. These positive granules were mostly round or ovoid in shape with variousdiameters. The present immunohistochemical results appears to support previous results suggesting that 5HT is located in such granules as alpha-granules anddense bodies.
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Salimnia, T., R. Ghandchi, K. Hughes, R. Chawla, M. A. Hicks, T. Marchewka i M. Shatila. "Pineapple Predisposing Pyrexia: Pineapple Induced Serotonin Syndrome". W American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a2256.

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Gauchel, N., K. Naber, K. Wolf, M. Mauler, C. Schönichen, P. Kröning, C. Bode, A. Braun i D. Duerschmied. "Platelet Serotonin in Arterial and Deep Vein Thrombosis". W 63rd Annual Meeting of the Society of Thrombosis and Haemostasis Research. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1680274.

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Jani, Sanket M., Lizbeth R. Lockwood i Mark M. Kadrofske. "Regulation of Intestinal Mucosal Wound Healing by Serotonin". W Selection of Abstracts From NCE 2016. American Academy of Pediatrics, 2018. http://dx.doi.org/10.1542/peds.141.1_meetingabstract.579.

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Raporty organizacyjne na temat "Serotonin"

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Rea, Michael A. Neuropharmacology of Circadian Phase Regulation by Serotonin. Fort Belvoir, VA: Defense Technical Information Center, grudzień 2002. http://dx.doi.org/10.21236/ada419071.

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Deng, Jianhao, jiaxing Zhang, QingXia Zhang i Guowei Zhong. Serotonin syndrome with dextromethorphan alone and in combination with other serotonergic drugs. a systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, maj 2022. http://dx.doi.org/10.37766/inplasy2022.5.0079.

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Review question / Objective: To assess the evidence for serotonin syndrome occurring in the context of dextromethorphan administration. To assess concurrent medication to see if there are associations with 1) other serotonergic medication. Condition being studied: It is uncertain whether use of dextromethorphan alone or in therapeutic doses can cause Serotonin syndrome (SS). Also, SS by dextromethorphan has not previously been systematically reviewed. Therefore, the main aim is to present a systematic review and summary of these studies.
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Reynolds, D. J., Paul L. Andrews i Christipher J. Davis. Serotonin and the Scientific Basis of Anti-Emetic Therapy,. Fort Belvoir, VA: Defense Technical Information Center, grudzień 1995. http://dx.doi.org/10.21236/ada304800.

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Rasenick, Mark M. Serotonin Signal Transduction in Two Groups of Autistic Patients. Fort Belvoir, VA: Defense Technical Information Center, październik 2012. http://dx.doi.org/10.21236/ada584868.

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Yan, Qingshan. Ethanol and Mesolimbic Serotonin/Dopamine Interactions via 5HT-1B. Fort Belvoir, VA: Defense Technical Information Center, marzec 2004. http://dx.doi.org/10.21236/ada426009.

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Rasenick, Mark M. Serotonin Signal Transduction in Two Groups of Autistic Patients. Fort Belvoir, VA: Defense Technical Information Center, grudzień 2013. http://dx.doi.org/10.21236/ada604752.

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Yan, Qingshan. Ethanol and Mesolimbic Serotonin/Dopamine Interactions Via 5-HT1B Receptors. Fort Belvoir, VA: Defense Technical Information Center, marzec 2006. http://dx.doi.org/10.21236/ada455523.

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Yan, Qingshan. Ethanol and Mesolimbic Serotonin/Dopamine Interactions via 5HT-1B Receptors. Fort Belvoir, VA: Defense Technical Information Center, marzec 2003. http://dx.doi.org/10.21236/ada416991.

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Yan, Qingshan. Ethanol and Mesolimbic Serotonin/Dopamine Interactions via 5-HT-1B Receptors. Fort Belvoir, VA: Defense Technical Information Center, marzec 2005. http://dx.doi.org/10.21236/ada443060.

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Mustapha, Faremi. Serotonin, Etonogestrel and breathing activity in murine Congenital Central Hypoventilation Syndrome. ResearchHub Technologies, Inc., kwiecień 2022. http://dx.doi.org/10.55277/researchhub.4id705aq.

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