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Data publikacji: 4 czerwca 2021

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1

Kaur, Baljit. "The conformational analysis of thyrotropin releasing hormone and its analogues". Thesis, Manchester Metropolitan University, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284878.

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2

Ouafik, L'Houcine. "Etude sur la biosynthèse de la Thyrotropin-Releasing Hormone (TRH) pancréatique". Grenoble 2 : ANRT, 1987. http://catalogue.bnf.fr/ark:/12148/cb37608585w.

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3

Ouafik, L'Houcine. "Etude sur la biosynthèse de la thyrotropin-releasing hormone (TRH) pancréatique". Aix-Marseille 2, 1987. http://www.theses.fr/1987AIX22004.

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4

Xiang, Shi Zhan. "Central control of the rat thyroid axis". Thesis, Brunel University, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320216.

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5

Ebiou, Jean-Claude. "Le rôle biologique de la thyrotropin-releasing hormone (TRH) dans le pancréas endocrine". Paris 7, 1992. http://www.theses.fr/1992PA077056.

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L'objectif de ce travail est la recherche du rôle biologique de la TRH pancréatique. La TRH a été initialement isolée de l'hypothalamus et caractérisée comme pGlu-His-ProNH₂. Elle a ensuite été détectée dans le pancréas endocrine désigne comme deuxième site de synthèse du peptide. La TRH est synthétisée à partir d'un précurseur de haut poids moléculaire. La maturation complète de celui-ci génèrerait 5 molécules de TRH, et 7 peptides de connexion. Nous avons montré que la TRH secrétée par le pancréas a les mêmes caractéristiques chromatographiques que le peptide synthétique. La sécrétion de la TRH pendant le développement est stimulé par le glucose et l'arginine, tandis que ces mêmes secretagogues inhibent la sécrétion chez l'adulte. Fait intéressant, la sécrétion de la TRH augmente avec l’âge, en dépit de la chute des contenus pancréatiques. Nous avons caractérise deux peptides de connexion de la prepro-TRH: prepro-TRH160-169 et prepro-TRH178-199, dans des ilots de Langerhans, et le prepro-TRH178-199 dans le milieu de sécrétion. Concernant le rôle biologique de la TRH pancréatique, nous avons montré que: la TRH exogène stimule la sécrétion basale du glucagon; l'immunoneutralisation de la TRH endogène secrétée par l'anticorps anti-TRH inhibe significativement la sécrétion du glucagon induite par l'arginine, la sécrétion de somatostatine est légèrement inhibée. Sur une fistule pancréatique, la TRH inhibe la sécrétion exocrine des protéines, bicarbonates, et du sodium. Les résultats préliminaires sur les cellules acinaires indiquent une absence d'effet TRH. L'effet TRH, observe in vivo, serait medié par le système nerveux central. Au cours du développement, la TRH n'a pas d'effet sur les secrétions d'insuline et glucagon. Nous pensons qu'elle agirait sur le processus de prolifération des cellules insulaires. La TRH stimule la sécrétion du glucagon des cellules alpha. Il serait intéressant de rechercher l'action biologique des deux peptides de connexion. La détermination du mécanisme d'action de la TRH pancréatique implique la caractérisation des sites de liaison spécifiques. Ce travail a été publié dans: Endocrinology 1992, 130(3):1371-1379; Endocrinology 1992, 131(2) (à paraitre en aout); prostate tumeurs 1991, (7):9-10 et 1992(9):6-7.

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6

Hart, G. R. "Mechanism of control of growth hormone release from the anterior pituitary : A role for thyrotropin-releasing hormone". Thesis, University of Sussex, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305765.

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7

Nguyen, Kim Thoa Thi [Verfasser]. "Thyrotropin releasing hormone (TRH) selectively stimulates human hair follicle pigmentation / Kim Thoa Thi Nguyen". Lübeck : Zentrale Hochschulbibliothek Lübeck, 2017. http://d-nb.info/114120309X/34.

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8

Carter, Rebecca Ann. "Thyroid Status in Exercising Horses and Laminitic Ponies". Thesis, Virginia Tech, 2005. http://hdl.handle.net/10919/35454.

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The objective of these studies was to contribute to the understanding and assessment of thyroid function in horses. The first study evaluated methods of assessing thyroid function in horses, including validation of an enzyme immunoassay (EIA) for measuring equine thyroid hormones and development and assessment of a thyrotropin releasing hormone (TRH) response test. Our data indicated that EIA is an acceptable method for the measurement of total (T) and free (F) thyroxine (T4) and triiodothyronine (T3) in equine plasma. Its measurements are not equivalent to values obtained by radioimmunoassay (RIA), but they can be calibrated to predict corresponding RIA values. A protocol was developed for TRH response tests involving administration of 1 mg TRH intravenously, with blood sample collection immediately before, 2.5, 5.0, and 24 h after administration. Analysis of plasma TT4, FT4, TT3, and FT3 revealed that the magnitude of hormone response was best approximated by the area under the curve of hormone plotted against time and by the absolute change in thyroid hormone concentration. Baseline concentrations, peak concentrations, and percent of baseline values were not as well able to predict the magnitude of hormone response. The second study assessed the effects of exercise and feed composition on thyroid status. Thirteen mature Arabian geldings, adapted to either a high sugar and starch (SS) or high fat and fiber (FF) feed, underwent 15 wk of exercise training followed by a treadmill exercise test. The TRH response tests performed before training, after training, and the morning after the exercise test revealed that the exercise test decreased the TT4 and FT4 response, whereas feeding of high levels of sugars and starches increased the response of TT3 and FT3. During the first four weeks of training, increased TT4 and FT4 concentrations occurred simultaneously with increased nonesterified fatty acid concentrations, decreased triglyceride concentrations, and increased insulin sensitivity. The increase in TT4 and FT4 may have provided the cellular signaling necessary for increased lipolysis and insulin sensitivity. These metabolic changes facilitate the increases in lipid and carbohydrate metabolism that are needed to fulfill the additional energy requirements of regular exercise. The third study assessed thyroid status in ponies with different laminitic histories. Total T4, FT4, TT3, and FT3 were measured during March and May 2004 in 126 ponies that were categorized as either previously laminitic (PL; n = 54) or never laminitic (NL; n = 72) and evaluated for current laminitis in May (CL; n = 13). Decreased concentrations of TT4 and FT4 were found in PL ponies when compared to NL ponies in March (P = 0.018, 0.020) and May (P = 0.018, 0.001). However, TT4 and FT4 concentrations in CL ponies were not different than concentrations in NL ponies in May (P = 0.82, 0.72), and when retrospectively separated out in March, were not different than NL ponies (P = 0.90, 0.84). Therefore, basal thyroid hormone concentrations are not useful as a predictor or hormonal characteristic of pasture-associated laminitis. The decreased TT4 and FT4 in PL ponies may be an indication of a response or compensation to laminitis and may facilitate the metabolic changes necessary to cope with the disease.
Master of Science

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9

Dromey, Jasmin Rachel. "Elucidating novel aspects of hypothalamic releasing hormone receptor regulation". University of Western Australia. School of Medicine and Pharmacology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0133.

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[Truncated abstract] G-protein coupled receptors (GPCRs) form one of the largest superfamilies of cell-surface receptors and respond to a vast range of stimuli including light, hormones and neurotransmitters. Although structurally similar, GPCRs are regulated by many diverse proteins, which allow the specific functions of each receptor to be carried out. This thesis focussed on two well-documented GPCRs, the thyrotropin releasing hormone receptor (TRHR) and gonadotrophin-releasing hormone receptor (GnRHR), which control the thyroid and reproductive endocrine pathways respectively. Although each of these anterior pituitary receptors is responsible for distinct physiological responses, both are integral to normal development and homeostasis. This thesis focused on three areas of GPCR regulation: ?-arrestin recruitment, transcription factor regulation and receptor up-regulation. The role of the cytoplasmic protein, ?-arrestin, has perhaps been previously underestimated in GPCR regulation, but it is now increasingly apparent that ?-arrestins not only inhibit further G-protein activation and assist in GPCR internalisation but also act as complex scaffolding platforms to mediate and amplify downstream signalling networks for hours after initial GPCR activation. It is therefore becoming increasingly important to be able to monitor such complexes in live cells over longer time-frames. ... Members of the E2F transcription family have been previously identified by this laboratory as potential GnRHR interacting proteins, via a yeast-2-hybrid screen and BRET. This thesis further investigated the role of E2F family members and demonstrates that a range of GPCRs are able to activate E2F transcriptional activity when stimulated by agonist. However, despite GnRHR displaying robust E2F transcriptional activation upon agonist stimulation, this did not result in any conclusive evidence for functional regulation, although it is possible E2F may modulate and assist in GnRHR trafficking. Furthermore it is apparent that E2F family members are highly redundant, as small effects in GnRHR binding and cell growth were only observed when protein levels of both E2F4 and E2F5 were altered. During the course of the investigation into the effect of E2F transcription on GPCR function, it was evident that long-term agonist stimulation of GnRHR had a profound effect on its expression. As this was explored further, it became clear that this agonist-induced up-regulation was both dose- and time-dependent. Furthermore, altering levels of intracellular calcium and receptor recycling/synthesis could modulate GnRHR up-regulation. In addition, an extremely sensitive CCD camera has been used for the first time to visualise the luciferase activity attributed to GnRHR up-regulation. Overall, this thesis demonstrates the complex nature of GPCR regulation. For the first time, long-term BRET analysis on ?-arrestin interactions with both classes of GPCRs has been examined in a variety of cellular formats. This has given valuable insights into the roles of phosphorylation and internalisation on ?-arrestin interaction. Additionally, this thesis has revealed that prolonged agonist exposure increases receptor expression levels, which has major implications for drug therapy regimes in the treatment of endocrine-related disorders and tumours.

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10

Sun, Yuh-Man. "Cloning and charaterisation of the Thyrotrophin-releasing hormone receptor and Gonadotrophin-relasing hormone receptor from chicken pituitary gland". Doctoral thesis, University of Cape Town, 1998. http://hdl.handle.net/11427/26973.

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The hypothalamic hormones, thyrotrophin-releasing hormone (TRH) and gonadotrophin-releasing hormone (GnRH), play pivotal roles in the growth and sexual maturation of chickens. In chickens, TRH regulates the release and synthesis of thyrotrophin (TSH) and also acts as a growth hormone-releasing factor. GnRH stimulates the release and synthesis of gonadotrophins (LH and FSH). TRH and GnRH are released and stored in the median eminence, and both hormones are transported into the pituitary gland via the hypophysial portal circulation. TRH and GnRH exert their physiological functions by binding to their specific receptors (TRH receptor and GnRH receptor, respectively) on the surface of cells in the pituitary gland. The activated receptors couple to guanine nucleotide-binding regulatory proteins (G proteins), Gq and/or G11, which in turn triggers the secondary messenger [1,2- diacylglycerol (DAG) and inositoltrisphosphate (IP3)] signalling cascade. The signalling generates the physiological effects of the hormones. The TRH-R and GnRH-R are members of G-protein coupled receptor (GPCR) family. The objective of this thesis was to clone and characterise the chicken TRH and GnRH receptors as useful tools for investigating the regulatory roles of TRH and GnRH receptors in the growth and sexual maturation of chickens. In addition, sequence information of the receptors would potentially assist in elucidating the binding sites and the molecular nature of the processes involved in receptor activation.

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11

Bertacchini, Eleonora. "Molecular study of stress system in the European sea bass (Dicentrarchus labrax): cloning of different components and effects of essential oil of Lippia alba during stress situation". Master's thesis, Alma Mater Studiorum - Università di Bologna, 2018.

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European sea bass (Dicentrarchus labrax) is one of the most important species in the Mediterranean aquaculture. In this context, fish are subjected to practices that activate the stress system and can adversely affect their health and welfare. To minimise the effects of stress on fish, investigators have begun to examine the use of natural products with anaesthetic properties that are more effective, safer and less expensive than the currently available synthetic drugs. The aim of the present study was to assess the effectiveness of the essential oil of Lippia alba (EOLA) to mitigate the stress response in D. labrax individuals disturbed by persecution. For this purpose, sea basses were subjected to 3 and 6 hours of stress procedure and sedated with two different concentrations of the EOLA, 25 and 50 μL L-1. Partial cDNA sequences of crhbp and trh genes were cloned and their mRNA expression, together with that of crh, pomc, star, nr3c1 and nr3c2, all stress-related genes of the hypothalamus-pituitary-interrenal axis, were analysed in different tissues. Results elucidated that the most conspicuous variations in gene expression were found out for crh at 6 hours, which pattern was inversely proportional to cortisol levels. This may indicate the existence of a negative feedback mechanism exerted by cortisol. Expression of mineralocorticoid and glucocorticoid receptors (nr3c1 and nr3c2) showed a trend that diverged in relation to the belonging tissue, but in hypothalamus it mirrored the variation of crh, highlighting again a role of cortisol in regulating gene expression during the stress response. Furthermore, an appreciable increment in trh mRNA occurred in every treatment after 3 hours, suggesting that this hormone can be involved in the stress response. The best concentration of EOLA in order to reduce stress is represented by 25 μL L-1. On the contrary, at 50 μL L-1, the oil can be itself a stressor and after 6 hours it loses its effectiveness and it degrades.

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12

Shortridge, Emily. "The Cryptic Peptides, Prepro-Thyrotropin Releasing Hormone 186-199 and 194-199, Suppress Anterior Pituitary Prolactin Secretion in vivo and in vitro". Thesis, The University of Arizona, 2012. http://hdl.handle.net/10150/221632.

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A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.
Prepro-thyrotropin releasing hormone (ppTRH)-176-199 is one of several peptide fragments cleaved during TRH synthesis and has been implicated as a regulator of neuroendocrine function. ppTRH 176-199 has been shown to acutely inhibit the stress-induced rise in ACTH, corticosterone (CORT), and prolactin (PRL) in the rat. The receptor for ppTRH 176-199 currently remains unknown. In this study we sought to characterize the active domain of ppTRH 176-199 and, using in vivo and in vitro approaches, determine its role in regulating anterior pituitary secretion of PRL. The 186-199, 194-199, and 186-191 amino acid fragments of ppTRH were administered I.P. to adult male Sprague-Dawley rats 15 min. prior to a 20 min restraint stress to determine the peptide’s active moiety in regulating prolactin secretion. Animals were euthanized and plasma was saved for assay of circulating PRL using enzyme immunoassay (EIA). ppTRH 186-199 significantly attenuated the stress-induced rise in prolactin in male rats in a dose-responsive fashion. This effect was mimicked by ppTRH 194-199 but not by ppTRH 186-191. At the highest dose (10 mg/kg BW), ppTRH 194-199 also reduced the stress-induced rise in plasma CORT. Additionally, in vitro studies were performed using the rat growth hormone (GH)/PRL –secreting MMQ cell line. MMQ cells were treated with ppTRH 186-199 and media was assayed for PRL levels. Cells were harvested and examined for changes in PRL mRNA. Within 30 minutes following treatment of estradiol-stimulated MMQ cells with ppTRH 186-199 there was a decrease in media levels of PRL compared to vehicle. Furthermore, in MMQ cells that were primed with 10nM estradiol for 48 hours there was an increase in media PRL levels, which was reduced following ppTRH 186-199 treatment. After 4 hrs of treatment, the inhibitory effect of ppTRH 186-199 on PRL secretion from MMQ cells was only seen on estradiol-stimulated cells. There were no effects of ppTRH 186-199 when examined after 24 hrs of treatment. There were no effects of ppTRH 186-199 or 194-199 of PRL mRNA levels. These data suggest that the carboxy terminal fragment of preproTRH 178-199 contains all the activity of this ppTRH cryptic peptide for regulation of PRL and corticosterone secretion. This suggests a potential moiety responsible for interaction with the peptide’s receptor. The inhibitory effect of ppTRH 186-199 and 194-199 on media PRL levels and not on mRNA synthesis implicates it as an effector of hormone secretion rather than protein synthesis. The short-lived duration of its effects supports a role as 6 an acute effector of the PRL system. The target receptor of the ppTRH 178-199 fragment remains uncertain. However the use of ppTRH 194-199 as a peptide bait may prove useful in identifying the receptor.

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13

Yamamoto, Akane. "Response of preterm infants with transient hypothyroxinaemia of prematurity to the thyrotropin-releasing hormone stimulation test is characterized by a delayed decrease in thyroid-stimulating hormone after the peak". Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/263539.

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14

Eymin, Cécile. "Étude des récepteurs de la sérotonine et de la thyrotropin-releasing hormone dans l'hippocampe humain normal et pathologique : mort subite du nourrisson et suicide". Lyon 1, 1993. http://www.theses.fr/1993LYO1T108.

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Trouslard, Jérôme. "Etude electrophysiologique du couplage excitation-secretion des cellules endocrines du lobe intermediaire de l'hypophyse : mise en evidence d'un effet excitateur medie par la thyrotropin-releasing hormone". Université Louis Pasteur (Strasbourg) (1971-2008), 1990. http://www.theses.fr/1990STR13072.

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Nous avons developpe une culture primaire de cellules endocrines du lobe intermediaire de l'hypophyse (cellules melanotropes) de porc sur lesquelles nous avons applique la technique electrophysiologique du patch-clamp. Nous avons caracterise un courant sodique tetrodotoxine sensible, trois courants calciques (t, l, n), un courant potassique retarde et un courant potassique transitoire. Ces courants s'integrent sous la forme de deux modes d'activite spontanee: une activite de potentiels d'action rapides de nature sodique et une activite de bouffees de potentiels d'action sodico-calciques. L'originalite de notre travail consista a mettre en evidence l'effet excitateur de la thyrotropin-releasing hormone (trh) sur le couplage stimulation-secretion de la cellule melanotrope de ce mammifere. La trh augmente la frequence de decharge de potentiels d'action, la secretion et la synthese hormonales. Au plan biochimique, nous confirmons le couplage du recepteur trh a une phospholipase c

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16

Sheward, William John. "Thyrotrophin releasing hormone, somatostatin and luteinizing hormone releasing hormone : aspects of their synthesis, release and actions". Thesis, University of Edinburgh, 1986. http://hdl.handle.net/1842/20183.

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Garnier, Marianne. "Contribution à l'étude du contrôle multifactoriel de l'activité sécrétoire des cellules mélanotropes : mécanisme d'action de l'acétylcholine, de la TRH et des agonistes adrénergiques". Rouen, 1998. http://www.theses.fr/1998ROUES025.

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Les cellules mélanotropes du lobe intermédiaire de l'hypophyse sont des cellules endocrines spécialisées dans la sécrétion de l'α-MSH, hormone qui, chez les amphibiens, joue un rôle majeur dans les phénomènes d'homochromie. Il est établi que l'activité sécrétoire des cellules mélanotropes est soumise à une régulation complexe faisant intervenir des neurotransmetteurs (tels que la dopamine, le GABA et la sérotonine) et des neuropeptides (tels que la TRH et le NPY). L'étude de l'effet et du mécanisme d'action de l'ACh dans les cellules mélanotropes montre que, chez la grenouille, l'ACh stimule la libération d'α-MSH via l'activation de récepteurs muscariniques de type M3 positivement couplés à la voie PLC/PKC par l'intermédiaire d'une protéine G insensible à la PTX. La réponse sécrétoire induite par la muscarine et à la TRH implique un influx calcique précoce sensible au Ni2+ qui est nécessaire à l'activation de la PLC. En revanche, les canaux calciques de type L, N, T, P ou Q ne jouent pas de rôle significatif dans le couplage stimulus-sécrétion induit par la muscarine. Chez le rat, contrairement à ce qui est observé chez la grenouille, l'ACh provoque une inhibition de la libération d'α-MSH par des LNI en périfusion. Cet effet s'exerce par l'intermédiaire de récepteurs muscariniques de type M2 négativement couplés à l'adénylyl cyclase via une protéine G sensible à la PTX. Par ailleurs, l'étude du contrôle catécholaminergique de la libération d'α-MSH hypophysaire montre que, en plus de la dopamine, la noradrénaline est présente dans le LNI de grenouille. L'adrénaline et la noradrénaline provoquent une inhibition puissante de la libération d'α-MSH par des LNI de grenouille en périfusion, mettant en jeu l'activation de récepteurs dopaminergiques (D2) et adrénergiques (α2 et β ). En conclusion, nos travaux soulignent la complexité de la régulation des cellules mélanotropes : (1) nous avons mis en évidence des effets opposés de l'ACh sur la libération d'α-MSH chez la grenouille et chez le rat ; (2) nous avons montré que, chez la grenouille, des mécanismes de transduction présentant des caractéristiques inhabituelles sont impliqués dans l'effet stimulateur de l'ACh et de la TRH ; (3) nous avons démontré l'existence d'un contrôle adrénergique/noradrénergique inhibiteur du lobe intermédiaire.

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18

Coggins, P. J. "Histidylproline : biochemical and behavioural studies on a thyrotrophin releasing hormone metabolite". Thesis, University of Newcastle Upon Tyne, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356142.

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Watson, Christopher David. "The role of thyrotrophin-releasing hormone in cognitive function in the rat". Thesis, University of Nottingham, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262166.

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20

Bristow, L. J. "A functional role for histamine in brain : Interactions with thyrotrophin releasing hormone (TRH)". Thesis, University of Nottingham, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.384327.

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21

Lighton, C. "Interactions between thyrotrophin-releasing hormone and 5-hydroxytryptamine in the rat central nervous system". Thesis, University of Nottingham, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.355293.

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22

Mabrouk, Mabrouk Mohamed. "Behavioural effects and neurochemical studies of a novel thyrotrophin-releasing hormone (TRH)-like peptide (FPP)". Thesis, University of Nottingham, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339688.

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23

Rojas, Asheebo. "KIR Channels in CO2 Central Chemoreception: Analysis with a Functional Genomics Approach". unrestricted, 2007. http://etd.gsu.edu/theses/available/etd-08032007-163450/.

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Thesis (Ph. D.)--Georgia State University, 2007.
Title from file title page. Chun Jiang, committee chair; Delon Barfuss, Deborah Baro, Teryl Frey, committee members. Electronic text (226 p. : ill. (some col.)) : digital, PDF file. Description based on contents viewed Nov. 1, 2007. Includes bibliographical references (p. 210-226).

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24

Waterfall, Alan H. "The development of in vivo methods to measure the neuropeptide thyrotrophin releasing hormone in the central nervous system". Thesis, University of Nottingham, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.358269.

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Drust, Debra Sue. "Thyrotropin-releasing hormone stimulated protein phosphorylation in GH₃ cells". 1985. http://catalog.hathitrust.org/api/volumes/oclc/13037265.html.

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Marrero, Diana. "Enhanced peptide transdermal diffusion of thyrotropin releasing hormone by iontophoresis". 1985. http://catalog.hathitrust.org/api/volumes/oclc/12717461.html.

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Thesis (M.S.)--University of Wisconsin--Madison, 1985.
Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 77-90).

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Dowty, Martin E. "Permeability of thyrotropin releasing hormone in rabbit buccal mucosa in-vitro". 1988. http://catalog.hathitrust.org/api/volumes/oclc/19054754.html.

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Thesis (M.S.)--University of Wisconsin--Madison, 1988.
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Dowty, Martin E. "Transport of thyrotropin releasing hormone in rabbit buccal mucosa in-vitro". 1991. http://catalog.hathitrust.org/api/volumes/oclc/25270907.html.

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Thesis (Ph. D.)--University of Wisconsin--Madison, 1991.
Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 174-193).

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29

Yard, Michael. "NEUROPROTECTIVE EFFECT OF THYROTROPIN-RELEASING HORMONE (TRH) AGAINST GLUTAMATE TOXICITY IN VITRO". Thesis, 2009. http://hdl.handle.net/1805/2005.

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Indiana University-Purdue University Indianapolis (IUPUI)
Acute and chronic activation of both ionotropic and metabotropic glutamate (glut) receptors is implicated in many neurodegenerative disorders including AD, dementia, epilepsy, stroke and neurotrauma. TRH and glut receptors (ionotropic & metabotropic) receptors are differentially coexpressed in granule and pyramidal neurons of the hippocampus. The author shows TRH to be protective when added to cultured pituitary adenoma (GH-3) cells and neuron-like pheochromocytoma (PC12) cells either prior to, during, or after glut-induced toxicity (Endo. Soc. Abs. 01), and also shows that the possible neuroprotective mechanism may involve heterologous downregulation of the metabotropic glut receptors, using superfused hippocampal slices and noting a reduction of Gαq/11 (SFN Abs. 02). He has also demonstrated that TRH protected against glut toxicity in fetal cortical cultures (Endo. Soc. Abs. 04). To extend these studies he used 14-day cultured rat fetal hippocampal neurons (Day E17) to determine if TRH is protective against toxicity induced by specific ionotropic and metabotropic glut agonists. Neuronal viability and integrity were assessed by trypan blue exclusion and LDH release after 18 hrs following 30 min exposure to glut agonists. Ten µM dihydroxyphenylglycine (DHPG, a Group 1 receptor agonist) + 30 µM N-methyl-D-aspartate (NMDA)-induced toxicity (42% vs contr. P<0.05); whereas, concurrent and continued treatment with 10 uM but not 1uM 3Me-HTRH resulted in less neuronal death and damage (86% vs contr P<0.05; 53% vs contr. P>0.05) respectively. DHPG treatment alone (10 µM) for 30 min. was non-toxic by both criteria (90% vs contr. P<0.05). The data suggest that TRH may be a selective modulator of glut-induced toxicity.

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Liu, Shy-Rong, i 劉詩蓉. "Interaction between triiodothyronine and ovarian steroids on the regulation of the release of thyrotropin and thyrotropin-releasing hormone". Thesis, 1994. http://ndltd.ncl.edu.tw/handle/94753419535004024562.

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31

TSAI, SHIOW-CHWEN, i 蔡秀純. "Effects of thyroid hormones on the release of thyrotropin-releasing hormone (TRH) and the response of thyrotropin and prolactin to TRH in rats". Thesis, 1992. http://ndltd.ncl.edu.tw/handle/97647378333674655421.

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32

Chen, Li-Min, i 陳利旻. "Comparison of Thyrotropin-Releasing Hormone Test and Thyroid-Stimulating Hormone Assay alone in Children with Neonatal Hyperthyrotropinemia". Thesis, 2013. http://ndltd.ncl.edu.tw/handle/95621025628898946496.

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碩士
高雄醫學大學
醫學研究所
101
Background: Thyrotropin-releasing hormone (TRH) test is useful for differentiating central and primary hypothyroidism, and is also valuable for diagnosing sub-biochemical hypothyroidism, an earlier stage than subclinical hypothyroidism, and usually the threshold of TRH test was set at 10~40 mIU/L. However, some experts are of the opinion that TRH test has a limited role in evaluating the early stage of hypothyroidism after the new generation of the thyroid-stimulating hormone (TSH) assay was applied to clinical use. The aim of this study was to investigate whether TRH test detects subclinical hypothyroidism earlier than TSH assay alone. Methods: This is a retrospective case analysis. Totally 228 children with thyroid eutopia who had neonatal hyperthyrotropinemia (HT) under levothyroxine supplement were collected between 1989 and 2008. Basal TSH level and TRH test were performed at the age of three to evaluate whether hypothyroidism developed after levothyroxine discontinued, and statistic analysis was performed. All the patients received follow-up visits for cognitive development and thyroid function after the TRH test to avoid over- or under-treatment. Results: In patients with thyroid eutopia and neonatal HT, 31.6% of them were still in status of hypothyroidism after the age of three if without supplement of levothyroxine. The basal TSH has good specificity (100%) for diagnosing euthyroidism, but with only 40.38% of sensitivity. When the basal TSH level was near the upper limit of normal range (4.5~8.5 mIU/L), the TRH test result correlated with hypothyroidism better (p = 0.033). The threshold of the TRH test set at 60 mIU/L had greater area under the curve compared with the previous threshold. Conclusions: Neonatal HT is a risk factor of hypothyroidism. We suggest the TRH test be administered in children with a basal TSH value near the upper limit of the normal range; the threshold of the TRH test may be set at 60 mIU/L. When the peak TSH level is above 60 mIU/L, the child is in hypothyroidism and usually needs levothyroxine supplement.

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Knight, W. David Overton J. Michael. "Cardiovascular and metabolic responses to central thyrotropin-releasing hormone during caloric restriction in rats". Diss., 2005. http://etd.lib.fsu.edu/theses/available/etd-11092005-145251.

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Thesis (M.S.)--Florida State University, 2005.
Advisor: J. Michael Overton, Florida State University, College of Human Sciences, Dept. of Nutrition, Food, and Exercise Sciences. Title and description from dissertation home page (viewed Jan. 26, 2006). Document formatted into pages; contains vii, 34 pages. Includes bibliographical references.

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34

ZHANG, GING-ZHONG, i 張慶忠. "Serum thyrotropin (TSH) and prolactin (PRL) responses to thyrotropin-releasing hormone (TRH) in patients with thyroid, adrenal and pituitary diseases". Thesis, 1986. http://ndltd.ncl.edu.tw/handle/79665522155501982441.

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35

Huang, Sheng-Wang, i 黃生旺. "Regulation of Ovarian Steroid Hormones and Thyroxine on the Secretion of Hypothalamic Thyrotropin-Releasing Hormone and Dopamine in Rats". Thesis, 1996. http://ndltd.ncl.edu.tw/handle/08347174788625148217.

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MO, FAN-YI, i 莫凡毅. "The interaction between acetylcholine and thyrotropin-releasing hormone on the secretion and gene expression of prolactin". Thesis, 1990. http://ndltd.ncl.edu.tw/handle/28166163504260496129.

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HUANG, SHENG-WANG, i 黃生旺. "Interaction between estradiol and thyroxine on the release of thyrotropin-releasing hormone into hypophysial portal blood". Thesis, 1990. http://ndltd.ncl.edu.tw/handle/17263751716442504131.

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38

LIU, ZHE-YU, i 劉哲育. "Effects of aging on the release of rat prolactin in response to thyrotropin-releasing hormone in vitro". Thesis, 1987. http://ndltd.ncl.edu.tw/handle/09388256591553296749.

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Lin, Feng-Ping, i 林豐平. "Mechanism of the potentiation effect of acetylcholine (ACh) on the thyrotropin releasing hormone (TRH)-induced c-fos mRNA expression". Thesis, 1995. http://ndltd.ncl.edu.tw/handle/03276673446680222249.

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碩士
國立陽明大學
生物化學研究所
83
GH3腦下腺垂體癌細胞株，經acetylcholine (ACh)24小時前處理後，會增強thyrotropin-releasinghormone(TRH)引發prolactin及C-fos基因表現。本篇進一步探討ACh對TRH刺激C-fos基因表現促進作用機轉。我們發現以TMB-8(細胞內鈣離子流動抑制劑)，thapsigargin(calcium/ATPase抑制劑，可以枯竭細胞內貯藏的鈣離子)，verapamil或nifedipine(specific L-type calcium channel blockeL)，EGTA(可螯合鈣離子)或Co2+(non-specificcalcium channel blocke)，與TRH共同處理細胞，結果ACh對TRH刺激c-fos基因表現仍有促進作用。KC1(增加鈣離子內流)可以刺激c-fos基因表現，且此作用被Ach促進。以高濃度PMA長期處理細胞以去除protein kinase C，發現ACh促進作用仍然存在，而低濃度PMA所刺激的c-fos基因表現，則可以被ACh所促進。進一步以HA1004為Ser/Thr kinase抑制劑處理細胞，發現無法去除ACh的促進作用，而cAMPanalog 8-Br-cAMP刺激c-fos基因表現，可以被ACh所促進。而在transfection實驗中ACh可以促進TRH刺激FC2 plasmid(c-fos promoter-CAT constructplasmid) CAT活性的表現。所以根據我們的結果，ACh的促進作用，可能發生在TRH刺激c-fos基因表現的下游蛋白，這個蛋白參與calcium、protein kinase C及cAMP對c-fos基因表現的調控。 We have previously showed acetylcholine (ACh) pretreatment potentiated thyrotropin-releasing hormone (TRH) induced c-fos gene expression in GH3 pituitary tumor cells. In the present study, we investigated the mechanisms underlying this potentiation effect. In the presence of TMB-8 to inhibit the intracellular calcium mobilization or thapsigargin to deplete intracellular calcium pool, the augmentation on TRH-stimulated c-fos mRNA expression by ACh persisted. Moreover, neither L-type channel blocker verapamil or nifedipine nor EGTA or Co2+ was able to inhibit the potentiation effect of ACh. KC1 increased c-fos mRNA expression, and this effect was potentiated by ACh. These results indicate that calcium is possibly not involved in the potentiation of ACh, but calcium stimulates c-fos mRNA expression were potentiated by ACh. Depleting cellular PKC by high dosage phorbol myristic acetate (PMA) have no effect on the potentiation of ACh. However, the PMA stimulated c-fos expression was potentiated by ACh. In addition, 8-Br-cAMP stimulated c-fos mRNA expression was potentiated in the ACh conditioned cells. The possibility that the augmentation by ACh was exerted at the transcriptional levels was examined with fusion gene construct composed of chloramphenicol-acetyl transferase (CAT) reporter gene driven by c- fos promoter (FC2 plasmid). Transfection of FC2 plasmid into GH3 cells show that TRH stimulated-CAT activity was increased by ACh pretreatment. Our results suggest that the signaling pathway downstream of calcium, PKC and cAMP appear to be responsible for the potentiation effect that eventually leads to accelerated c-fos gene transcription in the ACh conditioned cells.

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Chien-Hung, Pan, i 潘建宏. "Part 1 Subpopulation of the thyrotropin-releasing hormone- response anterior pituitary cells changed by aging Part 2 Effect of hypoxia on the expression of protein kinase C in rat brain". Thesis, 2003. http://ndltd.ncl.edu.tw/handle/88387306684698064762.

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碩士
中山醫學大學
生物化學研究所
91
Part 1 The anterior pituitary cell subpopulations of young and old Wistar male rat were tested by an experimental model of thyrotropin-releasing hormone (TRH)-induced increase in intracellular Ca2+ and were divided into five types: Type A, the cells with the reponse to TRH in low, media and high doses; type B, the cells response to either low or high doses TRH; type C, the cells only response to TRH low dose TRH; type D,the cells response to both media and high doses TRH; and type E,the cells response to only high dose TRH. Both young and old groups with high percentage of type A cells .The highly type A and type B were exist in young group(73.6 ±1.6% and 12.9±1.2%,respectively) compared with old group (68.3±1.1% and 4.4±1.0%,respectively).However, the percentages of type D and type E were significantly higher in old group(13.2±0.8% and 14.0±1.9% ;respectively) than in young group (7.6±1.2%and 4.7±0.8 %;respectively). These data indicated that the anterior pituitary cells in response to thyrotropin-releasing hormone may be partly shifted to low -sensitive cell types in aging. Part 2 To study the differential expressions of PKC isoforms in brain under hypoxia in conscious rats, the mRNAs were measured by RT-PCR. The male Sprague-Dawley rats were exposed in a simulated hypobaric chamber at 12 % O2 and 88% N2 for 8 h per day for 1 day or 4 days. The result showed that after hypoxia exposure the mRNA levels of some PKC isoforms were significantly decreased on day 1 and day 4: a (50% and 21%, respectively), d (40% and 17%, respectively), e (81% and 23%, respectively), q (64% and 12%, respectively) and l (88% and 28%, respectively), except PKC z was also significantly decreased but only on day 4 (74%), whereas PKC b and h were significantly increased on day 1 and day 4 (309% and 277% for b, respectively; and 241% 和 221% for h, respectively). Besides the PKC g was increased on day 1 (153%) and then decreased on day 4 (79%). All these findings suggested that the various expressions of PKC isoforms may be involved in the modulation of rat brain damage during hypoxia by different manner.

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Merta, Ladislav. "Organizace a mobilita receptorů spřažených s G proteiny v plasmatické membráně". Master's thesis, 2014. http://www.nusl.cz/ntk/nusl-332195.

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This diploma thesis deals with the analysis of structural and dynamic organization of thyrotropin releasing hormone receptor (TRH-R) and δ-opioid receptor (DOR) within plasma membrane (PM) in relation to the specific sub-compartments of PM denominated as domains or membrane rafts. Modern fluorescence microscopy techniques FLIM, FRAP and RICS were used for this purpose. The experiments were performed on the live cells derived from HEK293 cell line. To reach the main goal of this work, the integrity of PM structure was altered by depletion of cholesterol which was performed by incubation of cells with β cyclodextrin. Results clearly support our previously suggested idea that the vast majority of TRH-R is localized in non-raft regions of plasma membrane. This work also compared different modes of performance of FRAP and results obtained by FRAP and RICS because these methods are to some extent analogous. This is one of the first works that used the RICS approach to characterize the G protein-coupled receptors. In the second part of this work, the setup of transient transfection of the HEK293 cells with DOR-ECFP and DOR EYFP constructs was established. Simultaneously, the functionality of these constructs, i.e. the ability of DOR to activate the cognate G protein was determined. Powered by TCPDF (www.tcpdf.org)

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