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1

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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2

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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3

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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4

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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5

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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6

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

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7

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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8

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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9

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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10

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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11

Gharat, Laxmikant Atmaram. "Chemical studies on serotonin analogs". Diss., The University of Arizona, 1996. http://hdl.handle.net/10150/187502.

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The major focus of our research has been the design, synthesis and pharmacological evaluation of serotonin or 5-hydroxytryptamine (5-HT; 1) analogs. These include the conformationally restricted, rigid and semirigid analogs and those with a variety of different substituents, both electron donating and electron withdrawing, on the critically important indole 5-position. Two most interesting analogs in the tryptamine series are 5- carboxamidotryptamine (5-CT; 3a), a potent agonist at 5-HT₁ receptor and N,N-dipropyl- 5-carboxamido tryptamine (5-DPCT; 3b), a potent and selective agonist at the 5-HT₁ₐ receptor. We have found that this potency also extends to the semirigid analogs, 5- carboxamido-3-tetrahydropyridyl indoles (2a, 2b) (Agarwal et aI., 1993; Dahlgren et aI., 1995). In my research we decided to replace the 5-carboxyamido group by a group called the ɑ-fluoroethenyl or the ɑ-fluorovinyl group which was first proposed as an amide bond isostere in peptides (Allmendinger et aI., 1990). We synthesized 5-(ɑ-fluorovinyl)- 3-tetrahydropyridyl indoles (I, II) and 5-(a-fluorovinyl) tryptamines (III, IV) which could be potential bioisosteres of 2a, 2b, 3a and 3b. The a-fluorovinyl group was introduced on the indole 5-position using an "atypical" Heck reaction to prepare 5-(afluorovinyl) indole (5), the starting material for all the target compounds. We also performed some experiments to confirm the mechanism of the base-catalyzed direct condensation ofN-methyl-3- and -4-piperidones with indoles, a method employed for the synthesis of 3-tetrahydropyridylindoles I and II.
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12

Chang, Karin. "Platelets and Serotonin in Migraine". University of Toledo Health Science Campus / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=mco1279586929.

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13

Killam, Anne Louise. "Characterization of vascular serotonin receptors". Diss., The University of Arizona, 1990. http://hdl.handle.net/10150/184995.

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Determination of the physiologic roles of serotonin (5-HT) has long been hampered by the lack of compounds specific for certain of the 5-HT receptor subtypes. The objective of this dissertation was to characterize vascular serotonin receptors in certain arteries and to develop functional assays for the putative 5-HT₁(A) and 5-HT₂ receptors in vascular tissue to test novel compounds. Although 5-HT₁(A) receptor involvement in the 5-HT contraction of the canine basilar artery was previously reported, the 8-OH-DPAT (5-HT₁(A) specific agonist) EC₅₀ values in the canine, rabbit, guinea pig, and bovine basilar arteries studies were not consistent with the presence of 5-HT₁(A) receptors. Studies examining the 5-HT₂ selective antagonist ketanserin, several novel aryltryptamines with a range of affinities, and enantiomers of spiroxatrine, in the 5-HT-contracted rat aorta showed a good correlation between the aorta affinities and the affinities of these compounds at the [³H] ketanserin binding site (defined as 5-HT₂) in the rat frontal cortex. Comparison of the affinities of several known and novel compounds in the rat aorta and the rabbit femoral artery to the [³H] ketanserin site affinities in the frontal cortices of both species showed that the rabbit femoral artery 5-HT₂-like receptor was similar but not identical to either the rat aorta or the CNS sites from either species. The rabbit aorta and the rat femoral artery were then examined to determine if the 5-HT₂ receptor heterogeneity was species or vascular bed specific. The results from all four vascular tissues showed that no two tissues had identical responses to the compounds studied. The rat aorta appeared unique in the lack of agonist activity of RU24969 and the non-competitive antagonism of 5-HT by methysergide, but correlated to the CNS site for the affinities of all compounds. The major finding of the dissertation was the definitive evidence for vascular 5-HT₂ receptor heterogeneity; this subtype was previously thought to be homogeneous. Development of more selective compounds for 5-HT receptor subtypes may lead to greater understanding of the physiological roles of serotonin.
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14

Harkin, Emerson. "A Simplified Serotonin Neuron Model". Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/38533.

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15

Chee, Francis Craig. "Expression of Serotonin in the Development of Patiriella species (Echinodermata: Asteroidea) with Different Modes of Development". Thesis, The University of Sydney, 2000. https://hdl.handle.net/2123/24561.

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Serotonin expression was examined in the development of three species of seastars belonging to the genus Patiriella. These species represented three different modes of larval development, planktonic planktotrophic (P. regulars), planktonic lecithotrophic (P. calcar) and benthic lecithotrophic (P. exigua). Preneuronal serotonin-like immunoreactivity was detected in the ectoderm of the early gastrulae of P. regulars, and P. exigua up until the hatched brachiolarial stage. As serotonergic neurons appeared at the animal pole of the gastrulae of P. regulars, preneuronal serotonin expression was no longer evident in the ectodermal cells. These neurons were not associated with sensory-like structures such as an apical ciliary tuff. It is therefore suggested that serotonin in these neurons may be functioning as a trophic substance for their own growth and/or the development of the ciliated bands. These early serotonergic neurons also appeared to migrate to specific regions of the developing larva appearing to be the precursor neurons for the larval nervous system. Pharmacological depletion of serotonin, with the drug pchlorophenylalanine (L-PCPA), caused developmental abnormalities during gastrulation in P. regulars, P. calcar and P. exigua. These data suggested a morphogenetic role for serotonin during gastrulation. Drug treated P. exigua gastrulae also hatched prematurely, indicating a role for serotonin in the hatching process. Confocal immunofluorescence revealed ciliated serotonergic neurons in ganglia associated with the ciliated bands at the anterior and oral regions of the bipinnaria of P. regulars. Based on the disruption to feeding and swimming behaviour in P. regulars, induced by l -PCPA treatment, it is suggested that these ciliated serotonergic neurons function as sensory-like neurons in feeding and swimming behaviour. Reduction of serotonin content by L-PCPA also resulted in disruption to larval swimming in the lecithotrophic developer P. calcar.Serotonergic neurons were found in the brachiolarial arms and ciliated bands of P. regularis although immunoreactivity was absent from the adoral ciliated band of the mouth and the attachment disk. It is suggested that the absence of serotonergic neurons from the oral region reflects the changes in larval behaviour from a feeding state of the bipinnaria to the brachiolaria, which is primarily concerned with settlement behaviour. The brachiolarial arms and adhesive disk of the lecithotrophic developers, P. calcar and P. exigua contained numerous serotonergic neurons. The apical region of the serotonergic neurons of P. exigua and P. calcar contacted the exterior of the epithelium and it is suggested that these neurons function in sensing the substratum. The disruption of settlement behaviour in P. exigua by L-PCPA treatment also suggests a role for serotonin in attachment. Overall it appears that serotonin acts as a multifunctional neurochemical during different phases of development from the gastrula through to metamorphosis in Patiriella. Depletion of serotonin by l -PCPA was confirmed by reverse phase high performance liquid chromatography (rpHPLC). Irrespective of the morphological differences between the brachiolaria of the three species in this study, it appears that serotonergic neurons are conserved in like structures. A functional conservation of the role of serotonergic neurons in Patiriella is suggested.
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16

TAYLOR, ETHAN WILL. "THE DEVELOPMENT OF INDOLEAMINE DERIVATIVES SELECTIVE FOR SUBTYPES OF SEROTONIN RECEPTORS (TRYPTAMINE, BASILAR ARTERY, ANTAGONIST, ERGOLINE, SYNTHESIS)". Diss., The University of Arizona, 1985. http://hdl.handle.net/10150/188104.

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Central serotonin (5-hydroxytryptamine, 5-HT) receptors are classified into 5-HT₁ (defined by [³H]5-HT binding) and 5-HT₂ (defined by [³H]ketanserin binding). Antagonists selective for 5-HT₁ receptors or 5-HT₁(A) and 5-HT₁(B) subtypes are currently unavailable. To develop such antagonists, a study of derivatives of tryptamine (TRYP) (which are generally selective for 5-HT₁ sites) was undertaken. For amino-N-substituted TRYPs at 5-HT₁ sites, although overall potency decreases with increased N-alkyl substituent size (up to N,N-di-iPr), discrimination between subtypes of 5-HT₁ sites increases. Compounds such as N,N-di-iPr-TRYP (DIPT) and 3-(2-morpholinoethyl)indole (MEI) recognize 30% of [³H] 5-HT binding sites with high affinity (Ki<50 nM) , the rest with low affinity (Ki >4000 nM). For both the DIPT (agonist) and MEI (antagonist) series, incorporating 5-oxy substituents resulted in rank order to overall 5-HT₁ potency of 5 - OH>MeO=5H>BzO; however, the 5-oxy compounds lost the high-affinity recognition component shown by DIPT and MEI. Incorporation of an additional hetero-aromatic moiety gave amino-N-aryl substituted TRYPs (prototype AHR 1709). These were (1) highly selective for 5-HT₁(A) sites (Ki = 10 - 200 nM) over 5-HT₁(B) sites (Ki > 3000 nM), (2) potent at the 5-HT site & (3) vascular antagonists of 5-HT. Pharmacophoric differences between 5-HT₁, 5-HT₁(A) and 5-HT₂ sites were studied with rigid analogs. Racemic partial ergolines RU 27849 and RU 28306 showed diminished potency compared to TRYPs at 5-HT₁ sites, but were equipotent to homologous TRYPs at the 5-HT₂ site. At all three sites, 3-(tetrahydropyridyl)indoles (THPIs) were the most potent rigid analogs studied. A non-ergoline-like constrained analog of TRYP was synthesized and was even less potent than RU 27849 at 5-HT₁ sites, but was 4-5 times as potent as TRYP & RU 27849 at the 5-HT₂ site. While enhancing affinity for 5-HT₁ sites, the 5-MeO group can give reduced affinity for 5-HT₂ sites, thus enhancing 5-HT₁ selectivity. 5-Unsubstituted compounds may be best for 5-HT₂ selectivity. A study of 5-HT agonists in the canine basilar artery (CBA) suggests the contraction in vitro is mediated by a receptor similar to the 5-HT₁(A) binding site; 5-HT₂ receptors may also be present. Theoretical models for the production of apparent noncompetitive antagonism to 5-HT in the CBA are also examined. Syntheses of tryptamine derivatives and a conformationally constrained analog of TRYP are described.
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Rami, Martina [Verfasser], i Sabine [Akademischer Betreuer] Steffens. "Role of serotonin and antidepressants targeting serotonin transporters in atherosclerosis / Martina Rami ; Betreuer: Sabine Steffens". München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2018. http://d-nb.info/1175381616/34.

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18

Hamdan, Fadi F. "Serotonin biosynthesis and receptors in helminths". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0035/NQ64571.pdf.

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19

Bhagwagar, Zubin. "Serotonin, cortisol and vulnerability to depression". Thesis, University of Oxford, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.410616.

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20

Shaikh, S. "Serotonin and the rat adrenal gland". Thesis, University of Edinburgh, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383007.

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Serotonin (5HT) is an indoleamine with potent j vitro and in vivo effects on aldosterone biosynthesis in the adrenal zona glomerulosa of several species including Man and the rat. Its physiological role in the control of aldosterone secretion however, is not well understood. The purpose of these studies was to clarify its possible role in aldosterone biosynthesis using the rat as an experimental model. Attempts to localise 5HT within the adrenal gland using a specific monoclonal antibody to 5HT with the avidin-biotin detection technique, suggested, that serotonergic nerves are not present in the adrenal cortex although appreciable levels of 5HT were measured by HPLC in adrenal tissue ( 1.7 # 0.2 μg/ g wet weight). The storage and metabolism of 5HT in isolated zona glomerulosa cells and inner cortical and, medullary cells was investigated using [3 H]-5HT as a marker. Zona glomerulosa cells rapidly metabolised 5HT, whereas the inner zones were able to store or retain 5HT to a greater extent. Stimulation of steroidogenesis by 5HT however, was confined to the zona glomerulosa cells of the adrenal cortex. The interaction of 5HT with specific 5HT receptors was investigated by studying the effects of the 5HT antagonists, methysergide and ketanserin on the steroidogenic response to 5HT in isolated zona glomerulosa cell suspensions. Methysergide (10-6M) inhibited the corticosterone and aldosterone responses to 5HT (10-9M - 10-6)and angiotensin II (10-9M, 10-8M). In addition, it significantly inhibited the corticosterone response to ACTH. Ketanserin (10-6M) also inhibited the corticosterone and aldosterone responses to 5HT (10-9M, 10-8M) and All (10-9M, 10-8M) but did not affect ACTHstimulated steroidogenesis. Neither antagonist affected the steroidogenic responses to potassium. A change in dietary salt intake of rats did not lead to any significant change in either the blood levels or adrenal contents of 5HT. The in vitro- responsiveness of adrenal cells to 5HT however, was altered by changing the sodium status. An overall view of changing endogenous levels of 5HT in vivo in the rat was explored using the 5HT-depleting agent, PCPA and the immediate 5HT-precursor, 5-hydroxytryptophan (5HTP). Treatment with PCPA led to a decrease in blood 5HT levels and a loss of in vitro responsiveness to 5HT and All in subsequent preparations of zona glomerulosa cells. Treatment with 5HTP produced higher blood levels of 5HT and an enhanced responsiveness of subsequent preparations of zona glomerulosa cells. These studies suggest that 5HT from central and/or peripheral sources such as platelets or mast cells, could exert a tonic effect on aldosterone secretion from the rat adrenal zona glomerulosa, which is mediated by the activation of specific receptors for 5HT.
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Lima, João. "Serotonin transporter function and emotional behaviour". Thesis, University of Oxford, 2017. http://ora.ox.ac.uk/objects/uuid:ea4aa369-26e1-482a-9950-e027acca6f44.

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The serotonin transporter (5-HTT) is a key regulator of synaptic serotonin (5-HT), a monoamine that is significantly involved in the regulation of fear and anxiety processes. Importantly, low or null 5-HTT expression levels have also been associated with anxious and depressive phenotypes in several species. This remains controversial, however, with different research groups reporting conflicting results with most of the methodologies used so far to investigate whether such an association exists. An emerging 'neuroplasticity theory of 5-HT function' argues that low 5-HTT-expressing individuals, who are thought to have increased 5-HT availability, are not more vulnerable to anxious and depressive phenotypes per se but more sensitive to aversive and non-aversive life events. Subsequently, this increased sensitivity could lead to facilitated emotional learning in a 'for-better-or-for-worse' manner depending on their experiences in a given environment. This thesis aimed to investigate this further by testing knockout mice for the 5-HTT (5-HTTKO mice) in approach-avoidance conflict tests, social assays and discrimination learning tasks with negative and positive emotional stimuli. Additionally, in a subset of mice, altered basolateral amygdala (BLA) function during an aversive learning task was also investigated via recordings of neuronal and haemodynamic responses to emotional cues. The experiments reported here have shown that 5-HTTKO mice exhibit altered sensitivity towards emotionally-relevant negative and positive events and towards social influences. Moreover, 5-HTTKO mice exhibited superior aversive learning via augmented BLA function. However, the nature of the stimuli used in the experiments was crucial for the observation of such facilitated learning, given that learning about reward-predicting cues was not facilitated in 5-HTTKO mice. Overall, the results obtained in this thesis provide evidence for the neuroplasticity theory of 5-HT function at the behavioural and neurophysiological level. However, further studies are warranted to clarify the boundaries of this theory.
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Seibel, Yasmine. "The Role of Serotonin in Atherosclerosis". Doctoral thesis, Humboldt-Universität zu Berlin, 2020. http://dx.doi.org/10.18452/21818.

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Atherosklerose ist eine verbreitete Krankheit deren Pathogenese unzureichend erforscht ist. Bekannt ist jedoch, dass externe und interne Faktoren eine Rolle spielen. Die zugrunde liegenden Prozesse müssen genauer untersucht werden, um neue Therapieansätze zu entwickeln. Als Allroundtalent könnte Serotonin (5-HT) ein Kandidat sein, der eine entscheidende Rolle bei der atherosklerotischen Pathogenese spielt. Ob und wie dieses Hormon die Bildung atherosklerotischer Plaques, Makrophageninvasion, Verkalkung und Fibrose beeinflusst, war Gegenstand dieser Studie. Die vorliegende Studie ist die erste ihrer Art, die den neuartigen Ansatz von transgenen Doppel-Knockout-Mäusen verwendet, denen das Apolipoprotein E (ApoE) fehlt und, die das Schlüsselenzym für die periphere 5-HT-Synthese, Tryptophanhydroxylase 1 (Tph1), oder den primären 5-HT-Transporter (SERT) nicht bilden. Physiologie, Stoffwechselparameter und atherogene Prozesse wurden in ApoE/Tph1-/- und ApoE/Sert-/- Tieren mithilfe eines breiten Methodenspektrums untersucht und resultierten in einem umfassenden Überblick über die Wirkungsweisen von 5-HT auf Atherosklerose. Die 5-HT-Rezeptorverteilung ist unterschiedlich in Gefäßen von verschiedenen Mauslinien und in denen von Tieren mit Tph1-Defizienz, die in diesen Linien erzeugt wurden. Ferner weisen ApoE/Tph1-/- und ApoE/Sert-/- verschiedene Phänotypen auf: Tph1-Defizienz führt zu verminderter Zunahme des Körpergewichts, niedrigerem Plasmacholesterin und Leberparametern und erhöhtem Lebergewicht. Sert-Defizienz bedingt erhöhten Blutzucker, Plasmacholesterin und die Ausbildung größerer Plaques, sowie vermehrte Kollagenakkumulation. Die Langzeitgabe einer Western-Diät zeigte, dass Tph1-Defizienz schützende Wirkung auf den Lipidstoffwechsel hat, ein klarer Effekt auf die Atherogenese konnte nicht ermittelt werden. Zusammenfassend hebt diese Studie die komplexen Beziehungen vieler Faktoren während der Krankheit hervor. 5-HT spielt bei vielen dieser Faktoren eine Rolle, scheint jedoch nur eine schwache aber protektive Wirkung auf Atherogenese selbst zu haben.
Atherosclerosis is a common disease and its pathogenesis is only poorly understood. It’s known that external and internal factors play a role, but the exact processes need to be investigated more intensively to develop novel therapy approaches. As an all-round talent, serotonin (5-HT) might be a promising candidate to play a crucial role in atherosclerosis. If and how 5-HT affects atherosclerotic plaque formation, macrophage invasion, calcification and fibrosis was focus of this study. This study is the first of its kind using the novel approach of transgenic double knockout mice lacking the apolipoprotein E (ApoE, atherosclerosis model) and either the key enzyme in peripheral 5-HT synthesis, tryptophan hydroxylase 1 (Tph1) or the major 5-HT transporter, SERT. Physiology, metabolic parameters and atherogenic processes in ApoE/Tph1-/- and ApoE/Sert-/- animals were examined using a broad spectrum of methods and resulted in an extensive overview of how 5-HT might influence the pathogenesis of atherosclerosis. Most striking results of this study: 5-HT receptor distribution is altered in vessels of different background strains, and also in Tph1 deficient animals generated in these strains. Further, the examination of ApoE/Tph1-/- and ApoE/Sert-/- mice elucidated that both double knockouts exhibit different phenotypes: While Tph1 deficiency resulted in decreased bodyweight, plasma cholesterol and liver parameters and increased liver weight, Sert deficiency caused increases in blood glucose, plasma cholesterol, plaque size and collagen in plaques. Long term Western Diet application confirmed that Tph1 deficiency decreases weight gain and has protective effects on lipid metabolism, but a clear effect on atherogenesis could not be reported. Concluding, this study highlights the complex relationship between many factors acting on atherosclerotic pathogenesis. 5-HT plays a role in many of those factors, but seems to have only minor but protective effects on atherogenesis itself.
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Bourdon, David Milon. "Serotonin receptors in mammalian salivary glands /". free to MU campus, to others for purchase, 2001. http://wwwlib.umi.com/cr/mo/fullcit?p3012950.

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Bourdon, David M. "Serotonin receptors in mammalian salivary glands". free to MU campus, to others for purchase, 2001. http://wwwlib.umi.com/cr/mo/fullcit?p3012950.

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Corchs, Felipe D\'Alessandro Ferreira. "Serotonina e sensibilidade a estímulos relacionados ao trauma no transtorno de estresse pós-traumático remitido com inibidores seletivos de recaptura de serotonina". Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/5/5142/tde-24032009-171403/.

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INTRODUÇÃO: Apesar dos Inibidores Seletivos da Recaptura da Serotonina (ISRSs) serem a primeira escolha no tratamento do Transtorno de Estresse Pós-Traumático (TEPT) seu mecanismo de ação não é completamente compreendido. Possivelmente, um aumento na resiliência ao estresse esteja envolvido. Como a serotonina (5HT) ajuda a mediar as respostas ao estresse em outros transtornos ansiosos, o paradigma de Depleção de Triptofano Aguda (DTa) foi usado para diminuir a 5HT central em Pacientes com TEPT remitido com ISRSs. MÉTODOS: Dez pacientes com TEPT (diagnosticados pela Mini Entrevista Neuropsiquiátrica Internacional) que tiveram resposta completa com um ISRS (Escala de Impressões Clínicas Globais de Melhora 1-2 por pelo menos 3 meses) foram selecionados para o experimento. Os pacientes foram testados em duas ocasiões diferentes separadas por uma semana nas quais os pacientes receberam uma mistura contendo grandes aminoácidos neutros ou com (Depleção de Triptofano Falsa [DTf]; dia controle) ou sem triptofano (dia DTa). Auto relatos de ansiedade e humor, bem como medidas cardiovasculares, foram obtidos ao longo dos testes. Cinco horas e meia após a ingestão da mistura os pacientes foram re-expostos aos seus traumas através do procedimento de imaginação guiada de Pitman. RESLTADOS: Esses procedimentos provocaram elevados escores nas medidas avaliadas em ambos os dias, com respostas significativamente mais intensas no dia DTa conforme avaliado pelas Escalas Visuais Analógicas (DTa 47,57 [21,75] -v- DTf 20,71 [18,4]; p=0,001), Escala de Trauma de Davidson (29,4 [12,7] -v- 15,7 [7,79]; p=0,001), Inventário de Ansiedade de Spielberger versão Estado (28,9 [11,03] -v- 18,5 [10,13]; p=0,066, e Perfis de Estados de Humor (p<0,001). CONCLUSÕES: Esses dados são os primeiros a demonstrar que a depleção de 5HT piora as respostas subjetivas a re-experimentação de memórias traumáticas no TEPT e sugere que o aumento na função da 5HT induzida por ISRSs diminui os sintomas de TEPT, especialmente sob provocação, i.e. 5HT ajuda a mediar a resiliência ao estresse. Além de fornecer insights sobre o como os ISRSs funcionam no TEPT, esses dados também oferecem uma abordagem de potenciais novos tratamentos para esse transtorno
INTRODUCTION: Although Selective Serotonin Reuptake Inhibitors (SSRIs) are the first-line Posttraumatic Stress Disorder (PTSD) treatments their mechanism of action is unclear, but possibly improvement of stress resilience is involved. As serotonin (5HT) helps regulate stress responses in other anxiety disorders, the acute tryptophan depletion (aTD) technique was used to lower brain 5HT in SSRSs-remitted PTSD patients. METHODS: Ten patients with PTSD (Mini-International Neuropsychiatric Interview diagnosed) who had made a full recovery on SSRIs (Clinical Global Impressions Improvement Scale 1-2 for at least 3 months) were enrolled in the experiment. Patients were tested on 2 separate occasions a week apart - each session they received a drink containing large neutral amino acids either with (Sham Depletion [SD]; control day) or no tryptophan (aTD day). Self reports of anxiety and mood, as well as cardiovascular measures, were obtained throughout the tests. At 5.5 hours after the drink subjects were reexposed to their trauma using a modification of Pitmans imagery guided method. RESULTS: These procedures provoked elevated ratings on both days, with significantly more marked responses on the aTD day according to Visual Analogue Scales (aTD 47.57 [21.75] -v- SD 20.71 [18.4]; p=0.006), Davidson Trauma Scale (29.4 [12.7] -v- 15.7 [7.79]; p=0.001), Spielberger State Anxiety Inventory (28.9 [11.03] -v- 18.5 [10.13]; p=0.066, and Profile of Mood States (p<0.001). CONCLUSIONS: These data are the first to show that 5HT depletion worsens the subjective responses to reliving traumatic memories in PTSD and suggest that that SSRI-induced increases in 5HT function restrains PTSD symptoms, especially under provocation, i.e. 5HT helps mediate resilience to stress. As well as giving insights into how SSRIs work in PTSD, these data may also offer a translational approach to potential new treatments for this disorder
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Borg, Jacqueline. "Molecular imaging of the serotonin system in human behaviour /". Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-134-0/.

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Yan, Hongmei. "Stereoselective transport of drugs across the blood-brain barrier (BBB) in vivo and in vitro : pharmacokinetic and pharmacodynamic studies of the (S)- and (R)-enantiomers of different 5-HT₁A receptor agonists and antagonists /". Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2002. http://publications.uu.se/theses/91-554-5280-9/.

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Albinsson, Agneta. "Serotonin receptors in the regulation of prolactin release and some behaviors in the rat". Lund : Dept. of Zoophysiology, University of Lund, 1995. http://catalog.hathitrust.org/api/volumes/oclc/38865664.html.

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Mendelson, Scott Douglas. "Differential roles of serotonin receptor subtypes in the modulation of lordosis behaviour in the female rat". Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/29021.

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In 1985, Mendelson and Gorzalka proposed the dual role hypothesis of serotonergic modulation of lordosis behaviour. In this hypothesis it was proposed that serotonergic activity can either inhibit or facilitate lordosis behaviour. Specifically it was suggested that the lordosis-inhibiting effects of serotonin are mediated by activity at 5-HT₁ receptors, whereas lordosis-facilitating effects of serotonin are mediated by activity at 5-HT₂ receptors. The purpose of the following series of studies was both to confirm and to extend the dual role hypothesis. The intraperitoneal administration of the 5-HT2 antagonists pizotefin (1 mg/kg), cyproheptadine (1 mg/kg), metitepine (1 mg/kg), and ketanserin (1 mg/kg) were found to inhibit lordosis behavior in ovariectomized rats that had been primed with estradiol benzoate (EB) and progesterone (P). Pipamperone was ineffective. The 5-HT₂ agonist guipazine (3 mg/kg) was ineffective alone, but it reversed the inhibitory effects of pizotefin, cyproheptadine, and ketanserin. It did not reverse the effects of metitepine. The highly selective 5-HT₂ antagonist LY53857 (0.3 mg/kg) was also found to inhibit lordosis behaviour in female rats that had been primed with EB and P. The lordosis-inhibiting effect of LY53857 (1 mg/kg) in females primed with EB and P was reversed by quipazine (3 mg/kg). The nonselective 5-HT antagonist methysergide (7 mg/kg) was found to inhibit lordosis behavior 30 min after intraperitoneal administration to females treated chronically with EB, or with EB and P. However, methysergide was found to facilitate lordosis behavior 200 and 300 min after administration to female rats treated acutely with EB. In an analysis of dose response it was found that methysergide (0.02 - 7 mg/kg) administered 30 min prior to behavioural testing produced no facilitation of lordosis in females primed with EB. However, when administered 200 min prior to testing, methysergide (1 mg/kg) produced a significant facilitation of lordosis. The administration of the 5-HT₁ A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH DPAT) inhibited lordosis behavior in ovariectomized rats primed with EB. 8-OH DPAT was ineffective at 0.01 mg/kg, whereas inhibition occurred at the 0.03, 0.1, 0.3, 1.0, and 3.0 mg/kg doses. In an evaluation of the effects of 8-OH DPAT on the expression of male sexual behaviour by females treated chronically with testosterone, 8-OH DPAT ( 1 mg/kg) increased the number of females mounting and significantly increased mount frequency. The 5-HT₁ A agonists ipsapirone (0.1 mg/kg) and gepirone (0.3 mg/kg) facilitated lordosis in females treated with EB. When administered at higher doses, ipsapirone (3.0 mg/kg) and buspirone (3.0 mg/kg) inhibited lordosis in rats treated with EB. In females treated with EB and P, ipsapirone (> 1.0 mg/kg), gepirone (> 0.3), and buspirone (> 0.3) inhibited lordosis behaviour. The newly developed 5-HT₁ A antagonist BMY 7378 (0.2 mg/kg) facilitated lordosis behaviour in females treated with EB. However, this facilitation was no longer apparent at the 5 mg/kg dose. BMY 7378 (0.04 - 5 mg/kg) was ineffective in females primed with EB and P. The 5-HTTB agonist 1 -(3-trifluoromethylphenyl)piperazine (TFMPP, 0.2 -5 mg/kg) was found to facilitate lordosis in females treated with EB. In females primed with EB and P, TFMPP (5 mg/kg) produced a significant inhibition of lordosis. The 5-HT₁ B agonist m-chlorophenylpiperazine (MCPP, 0.04 - 5 mg/kg) was ineffective in females primed either with EB or with EB and P. The 5-HT₃ Antagonist ICS 205-930 (5 mg/kg) was found to facilitate lordosis behaviour, whereas the 5-HT₃ Antagonist MDL 72222 (0.05 - 5 mg/kg ) was found to be ineffective in females primed with EB. The results of these studies tend to confirm that serotonergic activity can either inhibit or facilitate lordosis behaviour. It is suggested that the lordosis-inhibiting effects of serotonin are mediated by activity at postsynaptic 5-HTTA and possibly 5-HT₃ Receptors. The lordosis-facilitating effects of serotonin are mediated by activity at 5-HT₂ and possibly presynaptic 5-HT₁ B receptors. Finally, it is suggested that activity at somato-dendritic 5-HT₁ A autoreceptors may mediate facilitatory effects of low doses of 5-HT₁ A agonists. In closing, there is a discussion of the implications these results might hold for the understanding of the effects of serotonergic drugs on human behaviour.
Arts, Faculty of
Psychology, Department of
Graduate
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Liwicki, Gemma Michele. "The design and synthesis of 5-HT₁B receptor antagonists". Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608202.

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Harrison, Amanda Ann. "The functional organisation of forebrain serotonin systems". Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263007.

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Ranganathan, Rajesh 1971. "Serotonin-dependent modulation of Caenorthabditis elegans behaviors". Thesis, Massachusetts Institute of Technology, 2001. http://hdl.handle.net/1721.1/80640.

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Abdul, Hussein Saba. "Conformational thermostabilisation of a mammalian serotonin transporter". Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609601.

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Alattas, Noor Abdulrahman S. "Polysaccharide-mediated formation of pigments from serotonin". Thesis, Tennessee State University, 2016. http://pqdtopen.proquest.com/#viewpdf?dispub=10119066.

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As a continuation of the research on the pigment formation from catecholamines, we studied the polysaccharide-mediated oxidation of serotonin and other 5-hydroxy indoles into pigmented substances. As for catecholamines, we observed that many polysaccharides promote the oxidation of such compounds, particularly in the presence of Cu (II). The same polysaccharides, e.g., carrageenan or fucoidan, which strongly promoted the oxidation of catecholamines, strongly promoted the oxidation of serotonin, leading to the formation of darkly colored pigments. The reactions were evaluated using RP-HPLC and size exclusion chromatography (SEC) as the main analytical techniques. SEC proved particularly informative as these analyses allowed us to monitor (1) the decline in the substrate, (2) the formation of low-molecular mass oxidation products, (3) the formation of polysaccharide-associated pigments, and (4) the formation of potential pigment-based nanoparticles. We observed that increased amounts of polysaccharide or Cu (II) increased the amount of pigment generated. However, other cations like Co(II), Ni(II), Mn(II), or Fe(II) had no or very little effect on the reactivity. Apart from serotonin, 5-hydroxy indole could serve as a substrate to generate polysaccharide-associated pigments. However, reactions with the related substrate, 5-hydroxy indole-3-acetic acid yielded a low molecular mass chromophore, but not any polysaccharide-associated pigments. Large-scale reactions were set up in an attempt to isolate and characterize any pigments that were generated. The reaction mixtures could readily be dialyzed and lyophilized to obtain polysaccharide-associated pigments. Pigments were evaluated using UV-Vis spectroscopy, SEC analysis, FT_IR spectroscopy, and atomic absorption spectroscopy to evaluate the amount of Cu remaining in the materials.

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Gow, Iain Frederick. "Development and application of assays for serotonin". Thesis, University of Edinburgh, 1987. http://hdl.handle.net/1842/18918.

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De, La Fuente Barrigon C. "Dopamine and serotonin metabolism in Parkinsonian models". Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10054116/.

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Parkinson’s disease (PD) is a neurodegenerative disorder caused by loss of dopaminergic neurons in the substantia nigra. Different pathogenic mechanisms have been implicated, including loss of mitochondrial complex I function and dysfunction of lysosomal glucocerebrosidase (GBA1) (Neumann et al., 2009; Schapira et al., 1990). Also, it has been hypothesised that serotonin metabolism could be affected in these patients due to the number of enzymes shared by both pathways (Albizu et al., 2011). This thesis considers the potential involvement of complex I and GBA1 in PD using HPLC analysis of changes in the extracellular levels of the metabolites of dopamine and serotonin, and the expression and activity of the enzymes of the dopamine pathway. Using SH-SY5Y cells, complex I deficiency was modelled using rotenone, and GBA1 deficiency was modelled using conduritol B epoxide (CBE). Inhibition of mitochondrial complex I or GBA1 significantly increased extracellular concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) and 5-hydroxyindoleacetic acid (5-HIAA), direct products of the degradation by monoamine oxidase (MAO) of dopamine and serotonin respectively. These results suggest increased MAO activity, providing evidence for the involvement of impaired complex I or GBA1 activity in the dopamine deficiency seen in PD. As MAO produces hydrogen peroxide as a side-product, its increased activity could enhance the oxidative stress present in PD (Dias et al., 2013). Therefore, intracellular GSH levels were quantified to determine whether the antioxidant mechanisms were affected, but no changes were observed. In addition to the main project, I collaborated with a number of groups to study monoamine metabolism in parkinsonian models. Also, the glycoprofile of cerebrospinal fluid (CSF) of patients with and without impaired dopamine metabolism was studied to explore the possibility of using glycans as pathologic biomarkers.
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Ordway, Gregory A. "The Inextricable Relationship Between Serotonin and Norepinephrine". Digital Commons @ East Tennessee State University, 2005. https://dc.etsu.edu/etsu-works/8664.

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Quested, Digby John. "Serotonin receptor mechanisms in anti-depressant action". Master's thesis, University of Cape Town, 2003. http://hdl.handle.net/11427/12577.

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Bibliography: leaves 221-270.
Serotonin neurones have been implicated in the pathophysiology and treatment of clinical depression to a greater degree than any other neurotransmitter. Additionally, serotonin pathways may playa role in the pathophysiology and treatment of eating disorders, anxiety states and schizophrenia. Molecular biological studies have confirmed pharmacological evidence suggesting the existence of multiple serotonin receptor subtypes and the genes for these receptors, as well as that of the serotonin transporter, have common polymorphic variants. To investigate the effect of repeated treatment with selective serotonin fe-uptake inhibitors (SSRI's) on the function of central 5-HT2C receptors. To assess the effect of polymorphic variation in the 5-HT2c receptor and serotonin transporter on functional responses to selective pharmacological challenge. To determine whether polymorphic variation in the 5-HT receptor and serotonin transporter influence the clinical response of patients with major depression to treatment with serotonergic antidepressants. To assess the effect of repeated treatment with selective serotonin re-uptake inhibitors (SSRI's) on the function of central 5-HT2c receptors I used the 5-HT2C receptor agonist, m-chlorophenylpiperazine (m-CPP) as a 5-HT2c probe in a neuroendocrine challenge paradigm. I used the same approach to assess whether polymorphic variation in the 5-HT2c receptor (serine vs cysteine substitution) was associated with differences in functional response to 5-HT2C receptor challenge. I then studied whether polymorphic variation in the serotonin transporter promotor region (long versus short form) was associated with differing functional responses to acute challenge with clomipramine, a tricyclic antidepressant with a high affinity for the serotonin transporter. Finally, I studied whether either of these polymorphic variants influenced the clinical response of patients with major depression to treatment with SSRI's and clomipramine. SSRI treatment significantly lowered the sensitivity of 5-HT2c receptors as predicted from animal experimental studies. However polymorphic variation in the 5-HTzc receptor did not significantly influence functional responses to m-CPP challenge. In contrast polymorphic variation in the serotonin transporter was associated with differing neuroendocrine responses to acute clomipramine challenge with greater prolactin release being seen in subjects with the long polymorphic variant. Neither the 5-HTzc nor the transporter polymorphisms correlated with clinical response to SSRI and clomipramine treatment in patients with major depression. The ability of SSRI's to produce a functional down-regulation of 5-HTzc receptors may be relevant to certain of their therapeutic effects. Polymorphic variation in the 5-HT2c receptor (serine vs cysteine) seems unlikely to explain functional differences in responses to 5-HTzc receptor challenge or antidepressant responses to SSRI treatment. In contrast variation in the serotonin transporter promotor is associated with differing functional responses to acute serotonin re-uptake blockade. However, this did not correlate with clinical response to longer-term SSRI treatment.
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Rasmussen, Fredrika. "The role of serotonin in animal personality". Thesis, Linköpings universitet, Biologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-138154.

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Interindividual differences in animal behaviour that are relatively consistent over time and context are referred to as animal personality. Personality has been recognized throughout the entire animal kingdom, in an array of species like molluscs, arthropods, fish, birds and mammals. The personality of non-human animals has been suggested to vary along five different axes, or continua; boldness-shyness, avoidanceexploration, activity, sociability and aggressiveness. Having a relatively fixed personality may seem nonadaptive compared to infinite behavioural plasticity so the individual would be able to respond adaptively to any changes in the environment. There can be physiological limitations to the phenotypic expressions of any trait, including behaviour. Variation in neuroendocrinology may thus explain why animals have personality. A candidate neurochemical that potentially proximately influences and forms personality, is serotonin (5- HT), one of the most omnipotent neurotransmitter of the animal body. In the many realms of the serotonergic system, there may arise individual differences which forms a proximate basis for differences in personality. In this review paper, I discuss the impact of the serotonergic system on a few different personality traits. Depending on the individual’s motivational state, serotonin can dampen or enhance aggression. Serotonin correlates negatively to anxious traits. Feeding behaviour is affected by serotonin in seemingly opposing directions. Overall, serotonin seem to underlie many behaviours that describe animal personality.
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Kolodziejczak, Marta. "Serotonin & developmental axonal refinement : microglia contribution ?" Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066073/document.

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La sérotonine a été impliquée dans le processus développemental de raffinement périnatal des connections synaptiques. D’autre rôle important est joue par des cellules immunitaires du cerveau, la microglie.Pendant ma thèse j’ai teste l’hypothèse qu’une interaction entre la microglie et la sérotonine est nécessaire pour l’établissement des circuits neuronaux correct dans le cerveau de la souris.Les résultats récents du laboratoire ont montré que la microglie exprime un des récepteurs à la sérotonine: le 5-HT2B. En utilisant comme model la ségrégation des axons retiennes dans le thalamus j’ai observé que la souris invalide pour ce récepteur présente des altérations anatomiques dans les régions des projections rétiniennes du thalamus.En parallèle, j’ai testé l’effet de la sérotonine sur la microglie. La libération locale de la sérotonine sur les coupes aigue du cerveau a un effet chemoattractant sur la microglie (2-photon microscopie).En plus, les analyses d'expression d’ARN de microglie dans une culture cellulaire primaire ont montres une augmentation de certains marqueurs d'activation dans la souris invalidée pour le récepteur 5-HT2B.Afin de tester quelle(s) cellule(s) sont responsable(s) pour les altérations observées dans le thalamus j’ai teste un nombre de souris avec une invalidation conditionnelle du récepteur 5-HT2B. Les résultats que j’ai obtenus pendant mon doctorat support l’hypothèse que la sérotonine interagit avec la microglie et que cette interaction pouvait être importante dans la maturation du cerveau
Serotonin, besides its functions as a neurotransmitter, actively participates in postnatal establishment and refinement of brain wiring in mammals. Another important role is played by the brain resident macrophages, microglia, in developmentally-regulated neuronal death as well as in synaptic maturation or elimination.During my thesis, I tested the hypothesis of cross-regulations between microglia and serotonin during postnatal brain development in a mouse model. The laboratory data show a major expression of the serotonin 5-HT2B receptor by postnatal microglia, suggesting that serotonin could participate in temporal and spatial synchronization of microglial functions. Using an in vivo model of synaptic refinement during early brain development, the maturation of retinal projections to the thalamus, I observed that Htr2B-/- mice present anatomical alterations of the projecting area of retinal axons into the thalamus.Parallelly, I tested the effects of serotonin on microglial cells. A local delivery of serotonin attracted microglial processes on acute brain slices (two-photon microscopy).Moreover, after comparing mRNA expression level in microglial primary cultures, we have found that some activation markers are upregulated in microglia from Htr2B-/-.In the second part of my PhD, by using a number of conditional Htr2B-/- mice, I investigated which cell type(s) could be responsible for the altered segregation of retinal axons in the thalamus of the total Htr2B-/- mice.Overall, my results support the hypothesis that serotonin interacts with microglial cells and that these interactions could participate in brain maturation
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Hiroi, Ryoko. "Effects of estrogen and serotonin on anxiety /". Thesis, Connect to this title online; UW restricted, 2008. http://hdl.handle.net/1773/9124.

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Zarpellon, Alessandro. "Platelet interactions with a-thrombin and serotonin". Doctoral thesis, Università degli studi di Padova, 2008. http://hdl.handle.net/11577/3425112.

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The aim of the first part of this thesis was to study platelets from people with essential thrombocytosis. Platelets from ET patients present several abnormalities. We focused on the abnormalities related with serotonin, in particular we wanted : 1) to determine the sub-cellular distribution of the neurotransmitter 2) to evaluate 5-HT transport in platelets either untreated or pre-incubated with reserpine, a known inhibitor of serotonin transport inside the dense granules 3) to establish whether the decreased accumulation of serotonin in pathological platelets was due to a decreased number of dense granules 4) to investigate the efficiency of the dense granules to accumulate basic amines; 5) to determine the amounts of ATP and Ca2+ contained in the dense granules 6) to evaluate the role of tyrosine kinases in the tranport of serotonin in platelets of MPDs subjects. 7) to analyze the serotonin-induced platelet activation (cytosolic [Ca2+] increase). The second part of this thesis performed at the Scripps Research Institute (La Jolla, CA) in the laboratory directed by prof. Z.M. Ruggeri was to precisely define the functional role of tyrosine sulfation in the a-thrombin binding to GpIba, a receptor present in platelets, that play a pivotal role in haemostasis and thrombosis.
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Lüttgen, Maria. "Serotonergic receptor subtypes in learning and memory : focus on 5-HT1A, 5-HT1B and 5-HT2A receptors /". Stockholm, 2004. http://diss.kib.ki.se/2004/91-628-6148-4/.

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Patocka, Nicholas. "Identification of a serotonin transporter and serotonin receptor in «Schistosoma mansoni»: a step towards better understanding the serotonergic system". Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114120.

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Among the top list of neglected tropical diseases sits schistosomiasis, a parasitic disease caused by the flatworm Schistosoma. The disease involves an intermediate snail host and the definitive human host with infection taking place through the skin in contaminated water, one of the reasons for its wide distribution. The diversity of the life cycle stages and the ability of the parasite to have adapted to quite different environments speak to the complexity of the organism. The underlying system that coordinates and controls all biological functions of the parasite is its nervous system. Signalling in the nervous system is accomplished by the release of neurotransmitters and signal transduction through specific receptors. Of the many neurotransmitters identified thus far in the parasite, serotonin (5-hydroxytryptamine: 5HT) is one of the most abundant. 5HT has been implicated in several biological functions in flatworms, including muscle contraction, motility and metabolism, but its mode of action is poorly understood. Here we provide molecular evidence for a serotonin-specific transporter (SERT) in Schistosoma mansoni as well as a serotonin specific receptor in the same organism. The transporter (SmSERT) was shown to share similar topology to SERTs from other organisms, namely 12 transmembrane regions with several predicted glycosylation sites. In a heterologous expression system, we show that it mediates the uptake of serotonin in a dose-dependent manner and is responsive to classical SERT inhibitors. The transporter is expressed in all life cycle stages tested (cercaria, schistosomulum, and adult) with upregulation occurring in the parasitic stages. Immunolocalization studies showed that the protein is expressed primarily in the nervous system of the parasite, both in central and peripheral neuronal structures. Using RNA interference (RNAi) to knockdown expression, we found strong increases in motility, suggesting that its primary function is in termination of serotonin signalling. The serotonin receptor (Sm5HTr) is the first as such cloned from parasitic flatworms. It shares homology with other 5HT receptors and most closely identifies with the 5HT7 class of receptors. Expression in mammalian cells found that it signals through upregulation of cAMP and not Ca2+. Immunolocalization in adults and larvae found that the receptor is enriched in the central and peripheral nervous system. Additional pharmacological assays using Sm5HTr agonists and antagonists suggest that the receptor may contribute to 5HT-induced stimulation of worm motility. Combined, these results show that there is a fully functional serotonergic system in the parasite S. mansoni and that these proteins play an important role in controlling signal transduction. The wide distribution of these proteins in the parasite nervous system and their apparent involvement in motor control makes them tempting targets for drug design.
Parmi la liste du haut des maladies tropicales négligées est assis la schistosomiase, une maladie parasitaire causée par le Schistosoma. La maladie implique un mollusque intermédiaires et hôte définitif de l'homme avec une infection en cours à travers la peau dans l'eau contaminée, l'une des raisons de sa large diffusion. La diversité des étapes du cycle de vie et de la capacité du parasite à avoir adapté à des environnements très différents parlent de la complexité de l'organisme. Le système sous-jacent qui coordonne et contrôle toutes les fonctions biologiques du parasite est son système nerveux. Signalisation dans le système nerveux est accompli par la libération des neurotransmetteurs et transduction du signal par récepteurs spécifiques. Parmi des nombreux neurotransmetteurs identifiés jusqu'à présent dans le parasite, la sérotonine (5-hydroxytryptamine : 5-HT) est l'un des plus abondants. 5HT a été impliqué dans plusieurs fonctions biologiques dans les vers plats, notamment contraction musculaire, la motilité et le métabolisme, mais son mode d'action est mal comprise. Ici nous fournir preuve moléculaire d'une transporteur de la sérotonine spécifique (SERT) au Schistosoma mansoni ainsi qu'un récepteur de la sérotonine spécifique dans le même organisme. Le transporteur (SmSERT) a été montré à partager la même topologie à SERT provenant d'autres organismes, à savoir 12 régions transmembranaire avec plusieurs sites de glycosylation prédits. Dans une expression hétérologue système, nous montrons qu'il négocie l'absorption de la sérotonine de manière dose-dépendante et est sensible aux inhibiteurs de SERT classiques. Le transporteur est exprimé dans toutes les étapes du cycle de vie testé (cercaria, schistosomula et adulte) avec regulation à la hausse survenant dans les stades parasitaires. Études immunolocalisation ont montré que la protéine est exprimée principalement dans le système nerveux du parasite, à la fois central et périphérique dans les structures neuronales. L'interférence ARN (ARNi) de rabattement d'expression, nous avons trouvé une forte augmentation de la motilité, suggérant que sa fonction principale est en cessation de signalisation de la sérotonine. Le récepteur de la sérotonine (Sm5htr) est le premier en tant que telle cloné à partir de vers plats parasitaires. Il partage homologie avec d'autres récepteurs 5HT et plus étroitement s'identifie à la classe des récepteurs 5-HT7. Expression dans des cellules de mammifères a constaté qu'il signale une regulation positive de l'AMPc et non de Ca2+. Immunolocalisation chez les adultes et les larves découvert que le récepteur est enrichi dans le système nerveux central et périphérique. D'autres essais pharmacologiques utilisant des agonistes et antagonistes suggèrent que le récepteur peut contribuer à la stimulation de la motilité du ver induite par la 5HT. Ensemble, ces résultats montrent qu'il existe un système sérotoninergique pleinement fonctionnel dans le parasite S. mansoni et que ces protéines jouent un rôle important dans le contrôle transduction du signal. La large diffusion de ces protéines dans le parasite système nerveux et leur implication apparente de commande de moteur fait d'eux des cibles tentantes dans la conception des médicaments.
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45

Traxler, Claudia [Verfasser], i Stefan [Gutachter] Unterecker. "Untersuchung serumpiegelabhängiger unerwünschter Arzneimittelwirkungen von selektiven Serotonin-Rückaufnahme-Inhibitoren sowie Serotonin-Noradrenalin-Rückaufnahme-Inhibitoren / Claudia Traxler ; Gutachter: Stefan Unterecker". Würzburg : Universität Würzburg, 2021. http://d-nb.info/1232647705/34.

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Kalkowski, Andreas. "Serotonin und seine lichtähnliche Wirkung im circadianen System der Ratte". [S.l. : s.n.], 2000. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB8862169.

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47

Manrique, Muñante Rubén. "Love: there is (bio)chemistry between us". Revista de Química, 2014. http://repositorio.pucp.edu.pe/index/handle/123456789/99292.

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El enamoramiento implica procesos bioquímicos en los que sustancias como neurotransmisores, neuromoduladores y hormonas  interaccionan con células nerviosas u otros órganos. Al estar enamorados, los niveles de dopamina aumentan generando atención, deseo y motivación en todo lo relacionado al ser amado. La serotonina, por el contrario, se presenta en concentraciones bajas en este estado. La oxitocina, por su parte, entra en juego cuando la demanda de dopamina no se logra suplir y es crucial al entablar relaciones de largo plazo. El entendimiento del mecanismo de la oxitocina en el ser humano es crucial no solo para el conocimiento académico sino también porque brinda luces para el tratamiento de algunos desórdenes psicológicos.
Romantic love involves biochemical processes in which substances such as neurotransmitters, neuromodulators and hormones interact with other nerve cells or organs. When being in love, dopamine levels increases, generating attention, desire and motivation in everything related to the beloved person. Serotonin, however, is present in low levels in this state. When the body does not supply the necessary amount of dopamine, oxytocin is released. Oxytocin is vital in long term relationships. Understanding the mechanism of oxytocin in humans is crucial not only for academic knowledge of the chemistry of love but also because it provides new lights for the treatment of some psychological disorders.
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48

Soares, Joacil Germano. "Delimita??o dos grupamentos serotonin?rgicos/n?cleos da rafe do moc? (kerodon rupestris): citoarquitetura e imunoistoqu?mica para serotonina". Universidade Federal do Rio Grande do Norte, 2010. http://repositorio.ufrn.br:8080/jspui/handle/123456789/17308.

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Made available in DSpace on 2014-12-17T15:37:01Z (GMT). No. of bitstreams: 1 JoacilGS_DISSERT.pdf: 4166780 bytes, checksum: d28a491081df0a86a997a1a2664b7535 (MD5) Previous issue date: 2010-12-28
Serotonin or 5-hydroxytryptamine (5-HT) is a substance found in many tissues of the body, including as a neurotransmitter in the nervous system, in which may exert varied post-synaptic actions. Inside the neuro-axis, the location of 5-HT neurons is almost restricted to the raphe nuclei of the brainstem, such that 5-HT-immunoreactivity can be considered a marker of the raphe nuclei. The raphe nuclei are located in the brainstem, at or near the midline. The serotonergic groups were originally alphanumerically classified as B1 to B9 towards caudorrostral in rats and can be divided into upper and lower groups. In this study the distribution of serotonergic neurons was studied using immunohistochemistry in the brain of the rock cavy (Kerodon rupestris), a species of rodent endemic to Northeastern Brazil. The cytoarchitectonic location of serotonergic neurons was established in series of adjacent coronal and sagittal sections stained by the Nissl method and immunohistochemistry for 5-HT. Thus, we defined the raphe rostral linear, caudal linear, dorsal, median, and paramedian pontine raphe nuclei, and B9 cluster, constituting the rostral group, and the interpositus, magnus, obscure and palidus, constituting the caudal part of the group, comparable to which has been described for other mammalian species
A serotonina ou 5-hidroxitriptamina (5-HT) ? uma subst?ncia encontrada em muitos tecidos do organismo, inclusive no sistema nervoso como neurotransmissor, onde pode exercer a??es p?s-sin?pticas variadas. Dentro do neuro-eixo, a localiza??o dos neur?nios 5-HT ? quase absoluta nos n?cleos da rafe do tronco encef?lico, de tal maneira que 5-HT neuronal pode ser considerada um marcador dos n?cleos da rafe. Os n?cleos da rafe est?o localizados no tronco encef?lico, na linha m?dia ou suas proximidades. Os grupamentos serotonin?rgicos foram originalmente classificados alfanumericamente como B1 a B9 no sentido caudorrostral no rato e podem ser divididos em grupos superior e inferior. Neste trabalho a distribui??o dos neur?nios serotonin?rgicos foi estudada com imunoistoqu?mica no c?rebro do moc? (Kerodon rupestris), uma esp?cie de roedor end?mica da regi?o Nordeste do Brasil. A localiza??o citoarquitet?nica dos neur?nios serotonin?rgicos foi estabelecida em s?ries de sec??es coronais e sagitais adjacentes submetidas a colora??o pelo m?todo de Nissl e imunoistoqu?mica para 5-HT. Assim, foram delimitados os n?cleos da rafe linear rostral, linear caudal, dorsal, mediano, paramediano e pontino da rafe e grupamento B9, compondo o grupo rostral, e os n?cleos interp?sito, magno, obscuro e p?lido, compondo o grupo caudal, compar?vel ao que j? foi descrito para outras esp?cies de mam?feros
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49

Hess, Marielle. "Entwicklung von MS-Bindungsassays für den Serotonin-Transporter". Diss., lmu, 2011. http://nbn-resolving.de/urn:nbn:de:bvb:19-138516.

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Spitzer, Nadja. "Identification and functional analysis of crustacean serotonin receptors". unrestricted, 2006. http://etd.gsu.edu/theses/available/etd-07192006-121025/.

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Thesis (Ph. D.)--Georgia State University, 2006.
Title from title screen. Donald H. Edwards, committee chair; Deborah J. Baro, co-chair; Charles D. Derby, Larry J. Young, committee members. Electronic text (182 p. : ill. (some col.)) : digital, PDF file. Description based on contents viewed May 21, 2007. Includes bibliographical references (p. 161-182).
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