Dissertations / Theses on the topic 'M1 muscarinic acetylcholine receptor'
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Thomas, Rachel. "Investigating allosteric activation of the M1 muscarinic acetylcholine receptor." Thesis, University of Leicester, 2010. http://hdl.handle.net/2381/9298.
Full textKim, Ju Young. "M1 muscarinic acetylcholine receptor regulation of endogenous transient receptor potential-canonical, subtype 6 (TRPC6) channels." Connect to resource, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1117570788.
Full textTitle from first page of PDF file. Document formatted into pages; contains xviii, 178 p.; also includes graphics. Includes bibliographical references (p. 163-178). Available online via OhioLINK's ETD Center
Schroeder, Lee Frederick. "An in vivo biosensor for neurotransmitter release and In situ receptor activity acetylcholine and the M1 muscarinic receptor /." Diss., [La Jolla, Calif.] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p3372798.
Full textTitle from first page of PDF file (viewed October 20, 2009). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 100-120).
Atkinson, Leone Sheila. "Development and characterization of herpes simplex virus type 1 vectors expressing m1 muscarinic acetylcholine receptors." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq25012.pdf.
Full textPrihandoko, Rudi. "An investigation into the pharmacology and regulation of the M1, M3 and M4 muscarinic acetylcholine receptors." Thesis, University of Leicester, 2013. http://hdl.handle.net/2381/28575.
Full textWard, Stuart David Charles. "The role of residues Tyr381 to Val387, in transmembrane domain six of the rat M1 muscarinic acetylcholine receptor, in agonist binding and receptor activation." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390625.
Full textBuffat, Maxine Guy Patrick. "Synthesis of selective M1 muscarinic receptor agonists." Thesis, University of Manchester, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.488787.
Full textSpalding, Tracy Anne. "Structural studies on the muscarinic acetylcholine receptor." Thesis, University College London (University of London), 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.315419.
Full textMadziva, Michael Taurai. "Mechanisms of M4 muscarinic acetylcholine receptor endocytosis." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619733.
Full textAslanoglou, Despoina. "Ligand regulation of muscarinic acetylcholine receptor organisation." Thesis, University of Glasgow, 2016. http://theses.gla.ac.uk/7048/.
Full textIarriccio, Silva Laura. "Allosteric interactions at the M3 muscarinic acetylcholine receptor." Doctoral thesis, Universitat Politècnica de Catalunya, 2008. http://hdl.handle.net/10803/6469.
Full textRadioligand binding experiments revealed that one mutant, K523E, had a profound potentiating effect on the binding of prototypical modulators like gallamine, strychnine, brucine and N-chloromethylbrucine, but had minimal effects on the binding of a number of orthosteric ligands, including [3H]N-methylscopolamine ([3H]NMS) and acetylcholine (ACh). The increase in affinity was found at both the unoccupied and [3H]NMS-occupied receptors, with up to 70 fold increases in affinity being observed. Switches from negative to positive cooperativity for some strychnine-related compounds were found.
At K523E, the affinities of the strychnine-related ligands were also increased up to 160 fold at the receptor-ACh complex, with up to 35 fold positive cooperativity being observed. Positive cooperativity of this magnitude is the highest that has been reported for M3 receptors.
The dramatic changes in cooperativities and affinities of allosteric ligands at K523E did not result in generation of the M1 phenotype. The K523Q data suggest that the large changes in K523E result from the introduction of the negatively charged glutamate residue and not the loss of the positively charged lysine. The effect of K523E seems to be solely on the binding of allosteric ligands and the transmission of the effects of their binding to the orthosteric site.
For the ligands acting at the gallamine site, all the effects of the allosteric modulators on ACh binding have been reproduced in functional studies, indicating that the allosteric modulation, seen in binding, is transmitted to the cellular response. A novel and unexpected finding is that WIN62,577 is an allosteric agonist at M3 muscarinic receptors and at K523E and N132G. The study also revealed that nanomolar concentrations of ACh may be present in assays of muscarinic receptor function and may give misleading interpretations of data. These artefacts were removed by preincubation with acetylcholinesterase, a control not previously used in functional studies of muscarinic receptors.
The sensitivity of the binding of both orthosteric and allosteric ligands to the composition of the binding assay buffer has also been investigated in detail. In a phosphate buffer of low ionic strength (PB) the affinity constants of all the compounds studied, both orthosteric and allosteric, were increased, relative to a Hepes buffer of higher ionic strength, except for WIN 62,577, an allosteric ligand which binds to a different allosteric site from the prototypical modulators, and SVT-40776 a new M3 selective antagonist, indicating their different modes of binding. Cooperativities have also been switched from negative to positive by changing buffer.
The two factors affecting the allosteric binding parameters of M3 receptors, PB and the mutation K523E, mutually potentiate each others effects. We have been able to obtain up to 10,000 fold changes in the affinity at the unoccupied receptor and 6400 fold increases in affinity at the ACh occupied receptor.
The possible location of K523, relative to other residues on the external loops of muscarinic receptors shown to be important for the binding of allosteric ligands, has been explored using different models based on the X-ray structures of rhodopsin and the â2 adrenergic receptor.
Blake, Allan David. "Functional characterization of a cloned Drosophila muscarinic acetylcholine receptor." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319493.
Full textBoxall, Donna Kirsty. "Muscarinic acetylcholine receptor signalling in model cells and smooth muscle." Thesis, University of Leicester, 1998. http://hdl.handle.net/2381/29959.
Full textSchlador, Michael Lee. "Agonist-dependent regulation of muscarinic acetylcholine receptor expression and function /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/6251.
Full textWylie, Paul. "Muscarinic acetylcholine receptor regulation of ERK and JNK in CHO cells." Thesis, University of Leicester, 2000. http://hdl.handle.net/2381/29924.
Full textNuckels, Richard J. "Ontogeny of muscarinic acetylcholine receptor expression in the eyes of zebrafish /." View online, 2006. http://ecommons.txstate.edu/bioltad/2.
Full textBorroto, Escuela Dasiel Oscar. "Human M3 muscarinic acetylcholine receptor protein-protein interactions: roles in receptor signaling and regualation." Doctoral thesis, Universitat Politècnica de Catalunya, 2008. http://hdl.handle.net/10803/22678.
Full textAkam, Elizabeth Claire. "The activation of guanine nucleotide binding proteins by muscarinic acetylcholine receptor subtypes." Thesis, University of Leicester, 1999. http://hdl.handle.net/2381/29919.
Full textJones, Kymry Thereasa. "The role of beta-arrestin in regulating the muscarinic acetylcholine type II receptor." Diss., Atlanta, Ga. : Georgia Institute of Technology, 2007. http://hdl.handle.net/1853/24815.
Full textCommittee Chair: Dr. Nael A. McCarty; Committee Co-Chair: Dr. Darrell Jackson; Committee Member: Dr. Alfred H. Merrill; Committee Member: Dr. Barbara D. Boyan; Committee Member: Dr. Harish Radhakrishna; Committee Member: Dr. Marion B. Sewer
Romero, Fernández Wilber. "Posttranslational modifications of human M3 muscarinic acetylcholine receptor: zooming in its functional implications." Doctoral thesis, Universitat Politècnica de Catalunya, 2011. http://hdl.handle.net/10803/110544.
Full textEl receptor muscarínico de acetilcolina subtipo M3 humano (M3R) regula importantes funciones en el sistema nervioso central y periférico, y está implicado en la fisiopatología de varias enfermedades neurodegenerativas y autoinmunes, lo que representa una atractiva diana terapéutica para la intervención farmacológica. Sin embargo, la falta de la información estructural sobre este receptor obstaculizado el desarrollo de nuevos y potente fármacos de gran selectividad y bajo efecto secundario. Tal información estructural, puede lograrse por medio de la experimentación con técnicas biofísicas que requieren grandes cantidades de receptor puro. Teniendo en cuenta que en condiciones fisiológicas la expresión de receptores acoplados a proteínas G (GPCR) es baja, la sobreproducción del receptor es un pre-requisito para que los estudios estructurales puedan ser realizados. Además, aunque se ha establecido que los GPCR sufren modificaciones post-translationales y que en los últimos años un significante número de reportes sugieren que estas modificaciones están estrechamente vinculadas a las funciones del receptor, poco se ha avanzado en el estudio de estas modificaciones en el campo de algunos GPCRs, como es el caso de M3R. En este estudio, nosotros describimos algunas estrategias para mejorar la expresión de los receptores muscarínicos en células de mamíferos garantizando unas correctas modificaciones post-translacionales. Además, hemos sido capaces de extraer altos niveles de receptor funcional a partir de células COS-7 con una combinación de detergentes, purificamos el receptor M3R cerca de la homogeneidad, mantenimiento de la totalidad de las propiedades biológicas encontradas en el receptor silvestre. En relación a las modificaciones post-translationales estudiadas, nuestros resultados proporcionan la primera evidencia del papel crítico de las cadenas de N-glicanos en la determinación de la localización de estos receptores, así como en la integridad celular. Además, nuestros datos revelan un importante papel de las modificaciones lipídicas de M3R en relación a la distribución del receptor en microdominios resistente a detergentes, así como en la regulación del receptor. En resumen, las estrategias utilizadas pueden contribuir al incremento de la expresión M3R. De esta forma los esfuerzos para la purificación del receptor a gran escala pueden ser iniciados. Para ellos, nosotros revelamos una posible estrategia. Además, proponemos los posibles sitios de N-glicosilación y S-acilación en el M3R expresado en células COS-7, y proporcionamos evidencias experimentales que avalan la implicación funcional de estas modificaciones en el papel del receptor.
Hornigold, David Charles. "Molecular studies of cross-talk between M2 and M3 muscarinic acetylcholine receptor subtypes." Thesis, University of Leicester, 2001. http://hdl.handle.net/2381/29927.
Full textMcKinnon, Lise Anne. "Developmental regulation of muscarinic acetylcholine receptor expression in embryonic chick heart and retina /." Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/6263.
Full textBee, Stephen. "Alanine-scanning mutagenesis of transmembrane helix 2 of the rat Mâ‚ muscarinic acetylcholine receptor." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397428.
Full textSandiford, Simone Laura. "Interaction of the G Beta Sub Five-RGS7 Complex with the Muscarinic Acetylcholine M3 Receptor." Scholarly Repository, 2009. http://scholarlyrepository.miami.edu/oa_dissertations/311.
Full textWang, Alice Wu. "Muscarinic acetylcholine receptor heterogeneity in the central nervous system of the tobacco hornworm, Manduca sexta /." Thesis, Connect to Dissertations & Theses @ Tufts University, 1998.
Find full textAdviser: Barry A. Trimmer. Submitted to the Dept. of Biology. Includes bibliographical references (leaves 92-105). Access restricted to members of the Tufts University community. Also available via the World Wide Web;
Dowling, Mark R. "Exploring agonist dependency of receptor-G protein-coupling and constitutive activity at muscarinic acetylcholine receptors." Thesis, University of Leicester, 2004. http://hdl.handle.net/2381/29941.
Full textSuharni. "Proteoliposome-based selection of a recombinant antibody fragment against the human M2 muscarinic acetylcholine receptor." Kyoto University, 2015. http://hdl.handle.net/2433/195961.
Full textRagheb, Fadi. "The M3 muscarinic acetylcholine receptor mediates p42mapk activation and c-fos mRNA expression in oligodendrocyte progenitors /." Thesis, McGill University, 1999. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=21627.
Full textThe M3 mAChR selective antagonist 4-DAMP and its irreversible analogue 4-DAMP-mustard, but not pirenzepine (M1) or methoctramine (M2/M4), prevented p42mapk activation and c-fos mRNA expression. Pretreatment with a phospholipase C (PLC) inhibitor U73122 but not the inactive analogue U73343 blocked both responses, while the phosphoinositide 3-kinase (PI3K) inhibitor wortmannin had no effect, suggesting the involvement of PLC but not PI3K.
In view of the fact that the M3 mAChR mediates p42mapk activation as well as c-fos mRNA expression, the MAPK Kinase (MEK) inhibitor PD 098059 was used to establish a link between both responses. PD 098059 pretreatment caused no significant attenuation in c-fos mRNA levels, demonstrating that this response may not be dependent on p42mapk activation. However, the phospholipase A2 (PLA2) inhibitors quinacrine and AACOCF3 abolished c-fos mRNA expression, implicating arachidonic acid and/or its bioactive eicosanoid metabolites.
In summary, these results demonstrate that in oligodendrocyte progenitors, the M3 mAChR is mediating both p42mapk activation and c-fos gene expression via PLC but not PI3K, whereby c-fos gene expression is not regulated by p42mapk but by PLA2.
Garriga-Canut, Mireia. "Control of neuron specific gene expression : transcriptional regulation of the Mâ†1 muscarinic acetylcholine receptor gene." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367599.
Full textPeng, Joyce Yaochun Kennedy Mary B. "Structure and function prediction of human muscarinic acetylcholine receptor 1, cation-pi studies, and protein design /." Diss., Pasadena, Calif. : California Institute of Technology, 2005. http://resolver.caltech.edu/CaltechETD:etd-05312005-114949.
Full textChirinda, Brian [Verfasser]. "The allosteric core region of the M2 muscarinic acetylcholine receptor : role for ligand selectivity and action / Brian Chirinda." Bonn : Universitäts- und Landesbibliothek Bonn, 2015. http://d-nb.info/107729042X/34.
Full textSchramm, Simon [Verfasser], and Michael [Gutachter] Decker. "Synthesis of Dualsteric Muscarinic M\(_1\) Acetylcholine Receptor Ligands and Neuroprotective Esters of Silibinin / Simon Schramm ; Gutachter: Michael Decker." Würzburg : Universität Würzburg, 2018. http://d-nb.info/1173088113/34.
Full textGibson, Hayley. "The Effect of Muscarinic Modulators on Cilia Structure and Function." University of Toledo Health Science Campus / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=mco1499104909617105.
Full textDickinson, Bryony. "An investigation into the mechanism of muscarinic acetylcholine receptor dependent long term depression in the CA1 region of the hippocampus." Thesis, University of Bristol, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.535163.
Full textAgnetta, Luca [Verfasser], Michael [Gutachter] Decker, and Pau [Gutachter] Gorostiza. "Novel Photoswitchable and Dualsteric Ligands Acting on Muscarinic Acetylcholine Receptors for Receptor Function Investigation / Luca Agnetta ; Gutachter: Michael Decker, Pau Gorostiza." Würzburg : Universität Würzburg, 2019. http://d-nb.info/1198682892/34.
Full textRisel, Philipp David [Verfasser], Peter [Akademischer Betreuer] Gmeiner, and Peter [Gutachter] Gmeiner. "Design and Synthesis of Novel Ligands for the M2 Muscarinic Acetylcholine Receptor / Philipp David Risel ; Gutachter: Peter Gmeiner ; Betreuer: Peter Gmeiner." Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2020. http://d-nb.info/1222739569/34.
Full textRagheb, Fadi. "The M3 muscarinic acetylcholine receptor mediates p42 [superscript]m [superscript]a [superscript]p [superscript]k activation and c-fos mRNA expression in oligodendrocyte progenitors." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0025/MQ50862.pdf.
Full textHeneghan, John F. "M1 Muscarinic Modulation of N-Type Calcium Channels: A Dissertation." eScholarship@UMMS, 2006. https://escholarship.umassmed.edu/gsbs_diss/255.
Full textKhan, J. "Investigation into the effects of specific muscarinic acetylcholine receptor antagonists on the myocardium in pre-clinical conditions of ischaemia reperfusion injury and oxidative stress model." Thesis, Coventry University, 2015. http://curve.coventry.ac.uk/open/items/3508a32c-8427-4ffe-9134-704a3e8c304b/1.
Full textKhoza, Kenneth. "Characterisation of the α2A-adrenoceptor antagonism by mirtazapine and its modifying effects on receptor signalling / Kenneth Khoza." Thesis, North-West University, 2004. http://hdl.handle.net/10394/673.
Full textThesis (M.Sc. (Pharmacology))--North-West University, Potchefstroom Campus, 2005.
Eager, Blenerhassit Edward. "The modulating effect of sildenafil on cell viability and on the function of selected pharmacological receptors in cell cultures / B.E. Eagar." Thesis, North-West University, 2004. http://hdl.handle.net/10394/611.
Full textThesis (M.Sc. (Pharmacology))--North-West University, Potchefstroom Campus, 2005.
Pontes, Carolina Nobre Ribeiro. "Influência da Angiotensina-(1-7) na sensibilidade colinérgica cardíaca de ratos normotensos e hipertensos." Universidade Federal de Goiás, 2018. http://repositorio.bc.ufg.br/tede/handle/tede/8940.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES
Previous studies suggested that the Angiotensin-(1-7) [(Ang-(1-7)] is able to modulate the cardiac sympathetic control and beta-adrenergic sensitivity. However, whether or not Ang-(1- 7) modulates the cholinergic activity in the heart remains unknown. The aim of this study was to evaluate the influence of Ang-(1-7) upon cholinergic sensitivity of hearts from normotensive and hypertensive rats. Wistar and Spontaneously Hypertensive Rats (SHR) were anesthetized with urethane and underwent catheterization of femoral artery and left ventricle to record the arterial and intraventricular pressure, respectively. Following, a dose-response curve of acetylcholine (ACh, 10, 20, 40 and 80 ng/Kg, i.v. into femoral vein) was performed in the absence or presence of Ang-(1-7) (7 x 10-12 mol/min), Mas receptor antagonist A-779 (7 x 10-11 mol/min) or Ang-(1-7)+A-779. Isolated hearts were perfused according to the Langendorff technique. Increasing concentrations of ACh (10-7 to 10-5 mol/L) were added to the hearts in absence or presence of Ang-(1-7), (2 x 10-11 mol/L), A-779, (2 x 10-10 mol/L), Ang-(1-7)+A-779, MrgD receptor antagonist, D-PRO (2 x 10-10 mol/L) or D-PRO+Ang-(1-7). ACh-induced vasorelaxation was assessed in absence or presence of Ang-(1-7) (2 x 10-11 mol/L or 2 x 10-10 mol/L). Ang-(1-7) attenuated the effect of ACh in decreasing the intraventricular systolic, dP/dt max and dP/dt min in anesthetized Wistar and SHR. These effects were blocked by A-779. Ang-(1-7) did not change the amplitude of the hypotensive effect evoked by ACh in Wistar or SHRs. In isolated hearts, Ang-(1-7) also attenuated the reduction of the intraventricular systolic pressure, dP/dt max and dP/dt min evoked by ACh. A-779 blocked the Ang-(1-7) effects in hearts from Wistar. A-779 or D-PRO did not modify the effects of Ang-(1-7) in hearts from SHR, but in presence of D-PRO, Ang-(1-7) effects were equipotent. Ang-(1-7) attenuated the vasorelaxation induced by ACh in aorta from SHR by only in SHR group. These data suggest that Ang-(1-7) exerts differential modulation of cardiac cholinergic sensitivity during experimental primary hypertension, which is independent on blood pressure.
Estudos prévios sugerem que a Angiotensina-(1-7) [(Ang-(1-7)] é capaz de modular o controle simpático cardíaco e sensibilidade beta-adrenérgica. Entretanto, ainda não se sabe se a Ang-(1-7) consegue modular a atividade colinérgica no coração. O objetivo deste estudo foiavaliar a influência da Ang-(1-7) na sensibilidade colinérgica cardíaca de ratos normotensos e hipertensos. Wistar e Ratos Espontaneamente Hipertensos (SHR) foram anestesiados com uretano e submetidos à canulação de artéria femoral e ventrículo esquerdo cardíaco para registro de pressão arterial e intraventricular, respectivamente. Em seguida, foi realizada uma curva dose-resposta de acetilcolina (ACh, 10, 20, 40 e 80 ng/Kg, i.v.) por infusão pela veia femoral. A infusão ocorreu na presença e ausência de Ang-(1-7) (7 x 10-12 mol/min), do antagonista do receptor Mas, A-779 (7 x 10-11 mol/min) ou de Ang-(1-7)+A-779. Os corações isolados foram perfundidos de acordo com a técnica de Langendorff e concentrações crescentes de ACh (10-7 a 10-5 mol/L) foram adicionadas aos corações na presença ou ausência de Ang-(1-7), (2 x 10-11 mol/L), A-779, (2 x 10-10 mol/L), Ang-(1-7)+A-779, antagonista do receptor MrgD, D-PRO (2 x 10-10 mol/L) ou D-PRO+Ang-(1-7). O vasorrelaxamento induzido pela ACh foi mensurado na presença ou ausência da Ang-(1-7) (2 x 10-11 mol/L ou 2 x 10-10 mol/L). Em Wistar e SHR anestesiados, a Ang-(1-7) atenuou o efeito da ACh na queda da pressão intraventricular sistólica, dP/dt máx, e dP/dt mín. Estes efeitos foram bloqueados pelo A-779. A Ang-(1-7) não alterou a resposta hipotensora da ACh em Wistar ou SHR. Nos corações isolados, a Ang-(1-7) também atenuou a redução na pressão intraventricular sistólica, dP/dt máx e dP/dt mín evocados pela ACh. O A-779 bloqueou os efeitos da Ang-(1-7) em corações de Wistar. O A-779 ou D-PRO, per se, não modificaram os efeitos da Ang-(1-7) em corações de SHR, mas na presença do D-PRO, a Ang-(1-7) apresentou efeitos similares. O vasorrelaxamento da aorta induzido pela ACh foi atenuado pela Ang-(1-7) apenas nos SHR. Estes dados sugerem que a Ang-¬(1-¬7) modula o sistema colinérgico cardíaco de forma diferente no modelo de hipertensão primária experimental e de maneira independente de ajustes na pressão arterial.
Obied, Taghrid Y. "Prediction of In-Vivo Antimuscarinic Activity (AMA) by In-Vitro Receptor Binding Assessment and PK/PD Modeling For Prototypical Drugs." VCU Scholars Compass, 2007. http://scholarscompass.vcu.edu/etd/1348.
Full textTribut, Florence. "Effets de l'axotomie sur les propriétés électrophysiologiques et pharmacologiques des récepteurs cholinergiques des cellules neurosécrétrices : les dorsal unpaired median (DUM) neurones du dernier ganglion abdominal de la blatte periplaneta americana L." Angers, 1994. http://www.theses.fr/1994ANGE0011.
Full textRoberts-Crowley, Mandy L. "Modulation of Cav1.3 L-Type Calcium Channels by Arachidonic Acid and Muscarinic M1 Receptors: A Dissertation." eScholarship@UMMS, 2007. https://escholarship.umassmed.edu/gsbs_diss/348.
Full textWarrier, Sunita. "cAMP BIOSENSORS AND SPATIOTEMPORAL cAMP SIGNALING IN ADULT CARDIAC MYOCYTES." Case Western Reserve University School of Graduate Studies / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=case1175718415.
Full textGreverath, Lena Maria [Verfasser]. "Untersuchung zur Bedeutung genetischer Polymorphismen des muskarinergen Acetylcholinrezeptors Typ 3 bei chronisch-entzündlichen Gallengangserkrankungen : Investigation of Muscarinic Acetylcholine Receptor Type 3 Gene Polymorphisms in chronic inflammatory bile duct diseases / Lena Maria Greverath." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2021. http://d-nb.info/1228860661/34.
Full textSihver, Sven. "Development of in vitro and ex vivo positron-emitting tracer techniques and their application to neurotrauma." Doctoral thesis, Uppsala universitet, Institutionen för neurovetenskap, 2000. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-485.
Full textBodenstein, Johannes. "Antagonism by selected classical irreversible competitive antagonists : an investigation into the proposed non-specific mechanisms involved / Johannes Bodenstein." Thesis, North-West University, 2003. http://hdl.handle.net/10394/92.
Full textThesis (Ph.D. (Pharmacology))--North-West University, Potchefstroom Campus, 2004.
Klawonn, Anna. "Molecular Mechanisms of Reward and Aversion." Doctoral thesis, Linköpings universitet, Centrum för social och affektiv neurovetenskap, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-143459.
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