Dissertations / Theses on the topic 'Opioid Receptors Signaling'
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ZHANG, SHENGWEN. "THE OPIOID RECEPTOR-LIKE RECEPTOR ORL1: SIGNALING AND INTERACTION WITH OPIOID RECEPTORS." University of Cincinnati / OhioLINK, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1029419843.
Full textZhang, Shengwen. "The opioid receptor-like receptor ORL1 signaling and interaction with opioid receptors /." Cincinnati, Ohio : University of Cincinnati, 2002. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=ucin1029419843.
Full textBasti, Vida. "Ligand biased signaling of opioid agonists forphosphorylation and regulation of μ -opioid receptors." Thesis, Uppsala universitet, Farmakologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-192584.
Full textXiang, Guoqing. "Signaling Through Homomeric and Heteromeric Cannabinoid CB1 receptors." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5683.
Full textHarrison, Charlotte. "Activation of multiple signaling pathways in cells expressing recombinant opioid receptors." Thesis, University of Leicester, 2000. http://hdl.handle.net/2381/29356.
Full textYu, Xiaochun, and 喻曉春. "Negative modulation of B-adrenoceptor by K-opioid receptor in the heart: signaling mechanisms and clinicalsignificance." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31241323.
Full textVelazquez-Marrero, Cristina M. "Modulation of Neuropeptide Release via Voltage-Dependent and -Independent Signaling in Isolated Neurohypophysial Terminals: a Dissertation." eScholarship@UMMS, 2008. https://escholarship.umassmed.edu/gsbs_diss/367.
Full textTumati, Suneeta. "Functional regulation of opioid receptor signaling." Diss., The University of Arizona, 2009. http://hdl.handle.net/10150/194989.
Full textOlson, Keith Mathew, and Keith Mathew Olson. "Atypical Opioid Interactions – Development of Selective Mu-Delta Heterodimer Antagonists, Clinical Opioids at Non-Mu Pain Targets and Endogenous Biased Signaling." Diss., The University of Arizona, 2017. http://hdl.handle.net/10150/626669.
Full textYu, Y. Joy. "Regulation of mu opioid receptor trafficking, signaling, and recycling in neurons." Diss., Search in ProQuest Dissertations & Theses. UC Only, 2009. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3378518.
Full textCooper, Andrew H. "The postnatal development of nociceptive and opioid receptor signalling pathways." Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/40839/.
Full textBlgacim, Nuria. "Molecular Control of the δ-opioid Receptor Signaling and Functional Selectivity by Sodium." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/37806.
Full textAsghar, Muhammad Junaid. "Studies on the biased signalling of some novel delta opioid receptor agonists." Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/40485/.
Full textSchmid, Benedikt [Verfasser], and Carsten [Gutachter] Hoffmann. "Molecular Signalling Mechanisms at the µ-Opioid Receptor / Benedikt Schmid ; Gutachter: Carsten Hoffmann." Würzburg : Universität Würzburg, 2020. http://d-nb.info/1204831513/34.
Full textXiaochun, Yu. "Negative modulation of B-adrenoceptor by K-opioid receptor in the heart : signaling mechanisms and clinical significance /." Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21415377.
Full textMadishetti, Sreedhar [Verfasser], Reinhard [Akademischer Betreuer] Wetzker, and Stefan [Akademischer Betreuer] Schulz. "PI3Kγ as a nodal point in μ-opioid receptor signaling / Sreedhar Madishetti. Gutachter: Reinhard Wetzker ; Stefan Schulz." Jena : Thüringer Universitäts- und Landesbibliothek Jena, 2012. http://d-nb.info/1028236689/34.
Full textSoftah, Abrar. "Multiple Cell Signaling Pathways Modulate the Cocaine-Induced Increase in Mu Opioid Receptor Protein Expression in PC12 Cells." Thesis, Abrar Ameen Softah, 2013. http://hdl.handle.net/10214/7189.
Full textSaudi Bureau in Canada
Tsisanova, Elena. "Characterization of extracellular signal-regulated Kinase1/2 (ERK1/2) signalling pathway at the μ-opioid receptor (MOPr)." Thesis, University of Bristol, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.688107.
Full textOkunomiya, Taro. "Generation of a MOR-CreER knock-in mouse line to study cells and neural circuits involved in mu opioid receptor signaling." Kyoto University, 2020. http://hdl.handle.net/2433/253202.
Full textGamaleldin, Mariam. "Non-canonical Signaling of μ-opioid Receptors." Master's thesis, 2021. https://doi.org/10.25972/OPUS-24032.
Full textNach dem „kanonischem“ Paradigma der Signaltransduktion akktivieren agonistbindende GPCR's nur dann die Adenylylcyclase, wenn sie sich in der Zellmembran befinden. Ist der Agonist länger gebunden führt dies meist zur Internalisierung des Rezeptors. Dies führt dazu, dass die Signaltransduktion beendet wird und andere Signalwege aktiviert werden. Jedoch haben einige neuere Studien gezeigt, dass zumindest einige GPCR's (z.B. der Thyreotropinrezeptor) auch nach Internalisierung weiter die Adenylylcyclase aktivieren. Das Ziel der vorliegenden Arbeit ist es kanonische Signaltransduktion von internalisierten μ Opioidrezeptoren (MORs) zu untersuchen, welche zu den Gi gekoppelten Rezeptoren gehören. Dazu wird ein Förster Resonanz Energie Transfer (FRET) Sensor für Cyclisches Adenosinmonophosphat (cAMP) benutzt, bekannt als Epac1-camps. Meine Resultate zeigen, dass die Inhibierung des cAMP Signal durch das Binden von DAMGO, einem MOR Agonisten, bestehen bleibt auch nachdem der Agonist ausgewaschen wurde. Unsere Hypothese ist, dass internalisierte Rezeptoren im endosomalen Kompartment, die DAMGO gebunden haben, die Ursache für das fortbestehende Signal verantwortlich sind. Um dies zu überprüfen habe ich Dynasore und Dyngo 4a benutzt. Beides sind Dynamin Inhibitoren von welchen man weiß, dass sie die Clathrin gesteuerte Endocytose unterbinden. Interessanterweise hat nur die Vorbehandlung mit Dynasore die Reaktion auf die MOR und die Adenylylcyclase Aktivierung mit Forskolin (FSK) verringert, jedoch nicht Dyngo 4a. Desweiteren hielt das durch DAMGO induzierte cAMP Signal selbst nach Zugabe von 30 M Dyngo 4a an. Diese Ergebnisse können ein Hinweis für einen komplexen Zusammenhang zwischen Clathrin gesteuerter Internalisierung und MOR Signaltransduktion sein. Jedoch braucht es weitere Experimente um den zugrundeliegenden Mechanismus der anhaltenden MOR Signaltransduktion zu beleuchten und um vollständig zu erklären ob MORs in der Lage für Gi Signaltransduktion im endosomalen Kompartment sind. (Übersetzt von Kerstin Seier)
Tsai, Hsin-Ju, and 蔡欣儒. "The Role of Opioid Receptors Signaling in Electroacupuncture-induced Cardioprotection in Rats." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/53382433111524419769.
Full text國立陽明大學
傳統醫藥研究所
102
Rationale: Our previous studies demonstrated that electroacupuncture (EA) increased myocardial GSK3 phosphorylation. Recent studies showed that GSK3 and opioid receptors activation can attenuate ischemia/ reperfusion (I/R) injury in rat hearts. However, the role of various opioid receptors (OR) subtypes in preconditioned EA-induced myocardial protection and the cross reaction with GSK3 remain unknown. Objective: We investigated the role of OR subtype signaling in EA-induced cardioprotection against I/R injury of the rat heart. Methods & Results: Male Spraque-Dawley rats were preconditioned by EA with/without various receptors antagonists such as opioid receptor (OR) subtype receptors (kappa OR, delta OR, and mu OR). The expressions of Akt, GSK3, and PKC-ε expression were analyzed by Western blotting. Our results showed that GSK3 and PKC-ε expression levels were significantly increased in the EA group compared to the sham group, which were blocked by pretreatment with specific antagonists targeting KOR and DOR, but not MOR subtype. In I/R model, rats randomly divided to sham EA (I/R alone), EA (I/R pretreatment with EA), EA+KOR left (EA with delta and mu OR antagonists), EA+KOR blocked (EA with kappa OR antagonist), EA+DOR left (EA with kappa and mu OR antagonist) and EA+DOR blocked (EA with delta OR antagonist). During ischemia and reperfusion, the rat's hemodynamic index, arrhythmia, mortality, infarction size, and serum CK-MB and troponin-I were evaluated. In our results, EA with/without OR antagonists did not change the mean blood pressure and heart rate. The incidence and duration of ventricular tachycardia and mortality during myocardial ischemia were significantly reduced by EA compared to sham EA. Moreover, the protection effects were complete reversed in EA+KOR blocked. Similarly, the infarction size was significantly reduced by EA and increased in EA+KOR blocked than sham EA. In the myocardial infarction marker, EA with/without did not significantly alter troponin-I. In RT-PCR analysis, the mRNA expression of opioid receptor subtypes were delta>kappa>mu. Moreover, the location of kappa OR in rat heart was in myocyte not vein analysis by immunofluorescence stain. Conclusion: The mechanism of EA-induced myocardial protection against I/R injury seems to involve multiple target pathways such as Akt, KOR and/or DOR signaling.
Moutelíková, Karolína. "Vliv chronického působení morfinu na přežití buněk po působení oxidativního stresu u neuroblastomové linie SH-SY5Y buněk." Master's thesis, 2018. http://www.nusl.cz/ntk/nusl-388352.
Full textΠαπακωνσταντίνου, Μαρία-Παγώνα. "Αλληλεπιδράσεις των επταελικοειδών υποδοχέων με διάφορες πρωτεΐνες. Χαρακτηρισμός νέων σηματοδοτικών μονοπατιών." Thesis, 2014. http://hdl.handle.net/10889/8440.
Full textΟpioid receptors (OR) (subtypes μ, δ, κ and NOP) belong to the superfamily of the Heptahelical G protein-coupled receptors (7TM or GPCRs), the largest class of receptors in the human genome and common targets for therapeutics. ORs mediate their responses in the nervous system via coupling to members of the Gi/Go proteins to regulate the activity of various effector systems. Opioids are the most potent analgesics but prolonged administration leads to phenomena of tolerance and dependence thus there is a great interest towards understanding of OR signalling in an effort to develop new drugs devoid of adverse effects. Extended observations have demonstrated that the cytoplasmic face of the ORs is critical in mediating their signal through interactions not only with G proteins but also with multiple other proteins. These regulatory proteins play distinct roles in the regulation of the OR signalling, and in the fine tuning of these receptors. Regulators of G protein signalling (RGS) proteins is a class of proteins that modulate G protein signalling events by directly interacting with Gα subunits and accelerating the GTP hydrolysis, thus reducing GPCR signalling towards their effectors. RGS can also interact with many GPCRs, effectors and auxiliary proteins thus playing a key role in the cell functions, making them highly attractive as pharmacological targets (Abramow-Newerly et al., 2006). Our previous in vitro studies have shown that a member of the B/R4 subfamily of RGS proteins such as RGS4 interacts directly with μ-OR and δ-OR within a conserved region in their C-termini (μ-CT and δ-CT), forming a helix VIII, as well as within the δ-third intracellular loop (δ-i3L). RGS4 associates with μ-OR and δ-OR in living cells and forms selective complexes with Gαi/o proteins in a receptor dependent manner. Expression of RGS4 in HEK293 cells attenuated adenylyl cyclase inhibition mediated by μ-OR and agonist-mediated ERK1,2 phosphorylation for both receptors (Georgoussi et al., 2006- Leontiadis et al., 2009), suggesting for the first time that RGS4 is a negative modulator of μ-OR and δ-OR signalling. To deduce whether similar effects also occur for the κ-opioid receptor (κ-ΟR) and define the ability of other members of the B/R4 subfamily of RGS proteins, such as RGS2, to interact with OR we generated fusion peptides encompassing the C-terminus of κ-OR (κ-CT). Results from pull down experiments indicated that RGS2 interacts with the κ-CT, the δ-CT and the δ-i3L but fails to interact with the μ-CT. RGS4-N-terminal domain is responsible for OR interaction. Mapping the sites of RGS2 interaction indicated that RGS2 interacts with the non conserved portion of the C-termini of ORs exhibiting a different docking site as compared to that of RGS4. Co-precipitation studies in living cells indicated that RGS2 and RGS4 associate with κ-ΟR constitutively and upon receptor activation and confer selectivity for coupling with a specific subset of G proteins in an RGS protein dependent manner. Expression of both RGS2 and/or RGS4, in 293F cells attenuated agonist mediated-adenylyl cyclase inhibition for κ-ΟR, but not δ-OR, with RGS2 exhibiting a more robust effect. RGS4 and RGS2 reduced κ-ΟR-mediated ERK1,2 phosphorylation whereas, RGS4 accelerated agonist-induced internalization of the δ-OR but not of the κ-OR. Collectively, our observations demonstrate that RGS2 and RGS4 are novel interacting partners and negative modulators of κ-ΟR and δ-OR signalling. These two RGS proteins display a differential modulatory effect in each signalling pathway tested and play a key functional role by conferring selectivity for both κ-OR and δ-OR coupling with a specific subset of G proteins. Therefore they can be considered as attractive new pharmacological targets to manipulate opioid receptors signalling.
Schmid, Benedikt. "Molecular Signaling Mechanisms at the µ-Opioid Receptor." Doctoral thesis, 2020. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-176850.
Full textNach wie vor stellen Opioide die wirkstärkste Gruppe von Medikamenten zu Behandlung starker Schmerzen dar. Auf molekularer Ebene sind alle heute gebräuchlichen Opioide Agonisten am μ-Opioidrezeptor. Der μ-Opioidrezeptor ist ein G-Protein-gekoppelter Rezeptor (GPCR) der Klasse A. GPCR zählen zu den häufigsten Zielstrukturen von Pharmaka. Sie sind membranständige Rezeptoren, die ihr Signal in erster Linie durch die Aktivierung von G-Proteine genannten GTPasen in die Zelle weiterleiten. Im Laufe des Signalprozesses wird der GPCR von GRK phosphoryliert, wodurch seine Affinität zu einer weiteren Gruppe von Signalproteinen, den sog. β-Arrestinen erhöht wird. Bindet ein β-Arrestin an den Rezeptor, beendet dies das G-Proteinsignal und veranlasst die Internalisierung des Rezeptors ins Zellinnere. Bisherige Forschung zeigte, dass das G-Proteinsignal des μ-Opioidrezeptors die erwünschte Schmerzlinderung vermittelt, wohingegen die Rekrutierung von β-Arrestin oftmals mit unerwünschten Wirkungen wie Obstipation, Toleranzentwicklung und Atemdepression in Verbindung gebracht wird. Neuere akademische und industrielle Forschung griff diese Erkenntnisse auf und erkundete die Möglichkeit, das G-Proteinsignal zu verstärken und zur gleichen Zeit die β-Arrestinrekrutierung zu inhibieren. Die theoretische Grundlage solcher Ansätze liegt im Konzept des biased agonism. Dieses berücksichtigt die Tatsache, dass verschiedene Liganden den Anteil eines bestimmten Signalweges am gesamten vom Rezeptor ausgehenden Signals beeinflussen kann und damit nicht nur rezeptor-, sondern sogar signalwegspezifische Signale möglich sein sollten. Die vorliegende Arbeit untersuchte eine Reihe von gängigen Opioiden auf ihre Fähigkeit hin, die einzelnen Signalwege spezifisch zu aktivieren und quantifizierte dies mit Methoden des Resonanzenergietransfers sowie der Proteinkomplementierung in lebenden Zellen. Die Phosphorylierung des Rezeptors ist ein zentrales Ereignis in der anerkannten Abfolge der Signalprozesse an GPCR. Daher wurde in einem weiteren Schritt die Expression der phosphorylierenden GRK erhöht und nach möglichen Auswirkungen auf die Selektivität der Signalwegaktivierung gesucht. Hierbei wurde detaillierte pharmakologische Profile von 17 Opioiden erstellt. Der Abgleich mit bekannten klinischen Wirkeigenschaften der Substanzen zeigte einen robusten Zusammenhang zwischen der Fähigkeit, G-Proteine zu aktivieren und der analgetischen Wirkstärke. Ligand bias, d.h. die signifikante Bevorzugung eines Signalweges gegenüber einem anderen durch einen Liganden, konnte für eine Reihe von Opioiden in lebenden HEK293-Zellen gezeigt werden, die den μ-Opioidrezeptor sowie β-Arrestine überexprimierten. Darüber hinaus konnte gezeigt werden, dass die zusätzliche Überexpression von GRK2 die pharmakodynamischen Eigenschaften nahezu aller Opioide grundlegend veränderte. In der Folge war jeder zuvor gezeigte ligand bias mit Ausnahme von Buprenorphin aufgehoben. Zusammenfassend stehen die folgenden drei Erkenntnisse im Vordergrund: (1) Gängige Opioide zeigen in einem gewissen Maß Selektivität zwischen den Signalwegen. (2) Ligand bias wird beeinflusst von GRK2-Expressionsleveln, welche zwischen Individuen, verschiedenen Gewebetypen oder auch im zeitlichen Verlauf variieren können. (3) Als einziges der untersuchten Opioide änderte Buprenorphin seine Signaleigenschaften durch die Überexpression von GRK2 nicht. Dies könnte als Anknüpfungspunkt in der Entwicklung neuer Opioide dienen, die keinerlei β-Arrestinrekrutierung bewirken und dadurch helfen könnten, unerwünschte Wirkungen in der Behandlung starker Schmerzen zu verhindern
Brejchová, Jana. "Úloha membránového cholesterolu v signalizaci delta-opioidního receptoru Korelace se strukturou plazmatické membrány." Doctoral thesis, 2014. http://www.nusl.cz/ntk/nusl-338451.
Full text"Mu-Opioid Receptor - pAKT Signaling in the Ventral Tegmental Area is Critical for the Behavioral and Cellular Consequences of Social Stress." Doctoral diss., 2015. http://hdl.handle.net/2286/R.I.29778.
Full textDissertation/Thesis
Doctoral Dissertation Neuroscience 2015
Bagheri, Haniyeh. "L'inhibition de la production d'AMPc est modulée différemment à court et long terme par l'internalisation du récepteur opioïde delta." Thèse, 2014. http://hdl.handle.net/1866/11815.
Full textOpioids are the most powerful analgesics but their prolonged use can cause the development of analgesic tolerance. The tolerance may be associated with the duration of response to cAMP. For this study, we used a biosensor based on Bioluminescence Resonnance Energy Transfer technology that provides measurements of cAMP levels as a function of real time. The aim of our study was to determine whether there is a correlation between the internalization profile of delta-opioid receptor (DOR) when stimulated by different ligands, with respect to the duration of signaling in the short-term (≤15 min) and long term (120 min). This evolution of the duration of cAMP inhibition is biphasic and is explained in part by the efficiency of ligands to promote Gαi activation and by the profile of internalization for each of the different ligands used in this study. For example, deltorphin II which displayed high efficiency to promote Gαi activation and internalization shows a more pronounced decline in cAMP response, unlike morphine which displayed low efficiency to promote Gαi activation, and a poor sequestration, displaying a minimal response decay of inhibition of cAMP. However, ligand ability to promote internalization of DOR does not explain the kinetic profile of a persistent inhibition of cAMP over a longer period of 120 min.
Charfi, Iness. "Étude du trafic du récepteur delta-opiacé suite à sa stimulation par différents agonistes." Thèse, 2012. http://hdl.handle.net/1866/8899.
Full textOpiates are among the most powerful painkillers to treat severe pain. Delta opioid receptor (DOR) agonists induce fewer side effects than mu opioid receptor agonists, which makes them a target of interest for the treatment of chronic pain. However, they induce tolerance to analgesia. Recent hypotheses suggest that drugs tolerance is the result of stabilization of ligand-specific conformations of the receptor, with distinct traffic properties such as internalization and/or recycling. In this context, we determined whether different DOR ligands differed with respect to their ability to induce signaling and receptor trafficking. Our results indicate that DPDPE and SNC-80 are the most effective drugs to inhibit the production of cAMP, followed by UFP-512, morphine and TIPP. Only DPDPE and SNC-80 manage to induce DOR internalization in HEK-293 cells. This effect is dependent on β-arrestin but not on GRK2 or PKC. Of these two internalizing agonists, only DPDPE allows the DOR to recycle back to the membrane of HEK-293 cells after recovery. DPDPE and SNC-80 also trigger similar DOR internalization in cortical neurons, and as observed in HEK293 cells only DPDPE allowed the receptor to recycle back to the membrane. This recycling capacity was suggested as a mechanism to protect against the onset of tolerance. These observations indicate that the DOR can undergo different regulations depending on the ligand bound to it. This property of functional selectivity of DOR ligands could be useful for the development of new opiates with longer lasting analgesic properties.