subject:(adenosine A1 receptor)

Universidade Estadual de Campinas

1. Oliveira, Caroline Candida de, 1987-. Efeitos mediados pelos receptores de adenosina no tecido adiposo branco durante a obesidade induzida por dieta hiperlipídica em camundongos: Effects mediated by adenosine receptors in white adipose tissue during high-fat diet-induced obesity in mice.

Degree: 2015, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/312469

► Abstract: Obesity, especially central (visceral), is related to low level systemic inflammation, by production of pro-inflammatory adipokines due to migration/activation of macrophages in white adipose… (more)

▼ Abstract: Obesity, especially central (visceral), is related to low level systemic inflammation, by production of pro-inflammatory adipokines due to migration/activation of macrophages in white adipose tissue (AT). Treatment with drugs that block this local inflammation results in improvement of many systemic parameters that are altered by obesity. Treatment with metotrexate in obese mice, an immunosuppressive drug, that inhibits adenosine cellular uptake, has resulted in significant metabolic improvement despite of the obesity maintenance. Thus, this study aimed to analyze a possible role of agonists of adenosine receptors A1 and A2A on metabolic and AT changes in mice with diet-induced obesity. Swiss mice were feed with commercial chow (CN) or high fat diet (HFD) for 12 weeks. In the last two weeks, mice were treated with CPA (selective A1 agonist, 0.05 and 0.1 mg/kg.day), CGS 21680 (selective A2A agonist, 0.1 and 0.5 mg/kg.day) or NECA (non-selective agonist, 0.005 and 0.01 mg/kg.day). Body weight, glucose blood levels and insulin tolerance test (ITT) were evaluated. AT biopsies were obtained for adipokines measurements using ELISA. Serum cytokines were evaluated by immunoassay Luminex. Expression of A1-R, A2A-R, JNK, VEGF, ERK, p38 MAPK and AMPK were assessed by Western blot. Macrophage infiltration was evaluated by immunochemistry (F4/80). Obese mice treated with CPA resulted in increased final weight and adiposity as compared with untreated obese controls. Animals treated with CGS 21680 and NECA had glucose levels reduced, but only treatment with CGS was able to reverse insulin resistance and reduce the insulin serum levels, suggesting an improvement of glucose homeostasis. All animal groups treated with agonists showed increased body metabolism. The lipolytic activity, evaluated by ex-vivo, was reduced in those animals treated with CPA 0.1, confirming previous published reports and indicating an anti-lipolytic activity mediated by A1 receptors. Animals treated with NECA, at lower dose, also showed reduced basal ex-vivo lipolysis. The macrophages infiltration, the monocyte chemoattractant protein (MCP) -1 production and tumor necrosis factor (TNF)-? were reduced in AT from animals treated with CGS. NECA and CPA also decreased MCP-1 expression in AT. The A2A receptor expression was unchanged in AT by obesity and the phosphorylation levels of p38 and ERK1/2 were increased by treatment with CGS. Systemically, only the production of plasminogen activator inhibitor (PAI)-1 was inhibited in CGS treated group. In conclusion, treatment of obese animals with adenosine agonists suggests that the A1 receptor activation results in anti-lipolytic effect that can cause weight gain, while A2A receptor activation results in anti-inflammatory effect on adipose tissue and improvement in glucose homeostasis. The use of non-selective agonist NECA results in isolated response, but it does not improve metabolic status, although we have observed a reduction of body weight and adiposity Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Gambero, Alessandra (advisor), Universidade Estadual de Campinas. Faculdade de Ciências Médicas (institution), Programa de Pós-Graduação em Farmacologia (nameofprogram), Araujo, Eliana Pereira de (committee member), Collares-Buzato, Carla Beatriz (committee member), Bosqueiro, José Roberto (committee member), Caperuto, Luciana Chagas (committee member).

Subjects/Keywords: Receptor A1 de adenosina; Receptor A2A de adenosina; Obesidade; Macrofagos; Tecido adiposo branco; Receptor, Adenosine A1; Receptor, Adenosine A2A; Obesity; Macrophages; Adipose tissue, White

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APA (6^th Edition):

Oliveira, Caroline Candida de, 1. (2015). Efeitos mediados pelos receptores de adenosina no tecido adiposo branco durante a obesidade induzida por dieta hiperlipídica em camundongos: Effects mediated by adenosine receptors in white adipose tissue during high-fat diet-induced obesity in mice. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/312469

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Oliveira, Caroline Candida de, 1987-. “Efeitos mediados pelos receptores de adenosina no tecido adiposo branco durante a obesidade induzida por dieta hiperlipídica em camundongos: Effects mediated by adenosine receptors in white adipose tissue during high-fat diet-induced obesity in mice.” 2015. Thesis, Universidade Estadual de Campinas. Accessed February 25, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312469.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Oliveira, Caroline Candida de, 1987-. “Efeitos mediados pelos receptores de adenosina no tecido adiposo branco durante a obesidade induzida por dieta hiperlipídica em camundongos: Effects mediated by adenosine receptors in white adipose tissue during high-fat diet-induced obesity in mice.” 2015. Web. 25 Feb 2021.

Vancouver:

Oliveira, Caroline Candida de 1. Efeitos mediados pelos receptores de adenosina no tecido adiposo branco durante a obesidade induzida por dieta hiperlipídica em camundongos: Effects mediated by adenosine receptors in white adipose tissue during high-fat diet-induced obesity in mice. [Internet] [Thesis]. Universidade Estadual de Campinas; 2015. [cited 2021 Feb 25]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/312469.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Oliveira, Caroline Candida de 1. Efeitos mediados pelos receptores de adenosina no tecido adiposo branco durante a obesidade induzida por dieta hiperlipídica em camundongos: Effects mediated by adenosine receptors in white adipose tissue during high-fat diet-induced obesity in mice. [Thesis]. Universidade Estadual de Campinas; 2015. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/312469

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Michigan

2. Sun, Daqing. Generation of mice with targeted disruption of the A1 adenosine receptor gene and their use in studies of renal function.

Degree: PhD, Molecular biology, 2001, University of Michigan

URL: http://hdl.handle.net/2027.42/128767

► Adenosine exerts a wide range of effects throughout the body, and these actions are mediated by four subtypes of adenosine receptors (A1, A2a, A2b and… (more)

Subjects/Keywords: A1 Adenosine Receptor; Adenosine A1 Receptor; Cardiac Cells; Function; Gene; Generation; Mice; Renal; Studies; Targeted Disruption; Use

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sun, D. (2001). Generation of mice with targeted disruption of the A1 adenosine receptor gene and their use in studies of renal function. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/128767

Chicago Manual of Style (16^th Edition):

Sun, Daqing. “Generation of mice with targeted disruption of the A1 adenosine receptor gene and their use in studies of renal function.” 2001. Doctoral Dissertation, University of Michigan. Accessed February 25, 2021. http://hdl.handle.net/2027.42/128767.

MLA Handbook (7^th Edition):

Sun, Daqing. “Generation of mice with targeted disruption of the A1 adenosine receptor gene and their use in studies of renal function.” 2001. Web. 25 Feb 2021.

Vancouver:

Sun D. Generation of mice with targeted disruption of the A1 adenosine receptor gene and their use in studies of renal function. [Internet] [Doctoral dissertation]. University of Michigan; 2001. [cited 2021 Feb 25]. Available from: http://hdl.handle.net/2027.42/128767.

Council of Science Editors:

Sun D. Generation of mice with targeted disruption of the A1 adenosine receptor gene and their use in studies of renal function. [Doctoral Dissertation]. University of Michigan; 2001. Available from: http://hdl.handle.net/2027.42/128767

Dalhousie University

3. Liu, Jean. Further Studies in Adenosinergic and Monoaminergic Mechanisms of Analgesia by Amitriptyline.

Degree: MS, Department of Pharmacology with Neuroscience, 2012, Dalhousie University

URL: http://hdl.handle.net/10222/15329

► In this thesis, rodent models of chronic pain were used to explore analgesic mechanisms that may potentially be engaged in spinal and peripheral compartments by… (more)

Subjects/Keywords: amitriptyline; persistent post-surgical pain; adenosine A1 receptor; serotonin 5-HT7 receptor; formalin test; antinociception; spared nerve injury; preventive analgesia; antidepressants; pain

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Liu, J. (2012). Further Studies in Adenosinergic and Monoaminergic Mechanisms of Analgesia by Amitriptyline. (Masters Thesis). Dalhousie University. Retrieved from http://hdl.handle.net/10222/15329

Chicago Manual of Style (16^th Edition):

Liu, Jean. “Further Studies in Adenosinergic and Monoaminergic Mechanisms of Analgesia by Amitriptyline.” 2012. Masters Thesis, Dalhousie University. Accessed February 25, 2021. http://hdl.handle.net/10222/15329.

MLA Handbook (7^th Edition):

Liu, Jean. “Further Studies in Adenosinergic and Monoaminergic Mechanisms of Analgesia by Amitriptyline.” 2012. Web. 25 Feb 2021.

Vancouver:

Liu J. Further Studies in Adenosinergic and Monoaminergic Mechanisms of Analgesia by Amitriptyline. [Internet] [Masters thesis]. Dalhousie University; 2012. [cited 2021 Feb 25]. Available from: http://hdl.handle.net/10222/15329.

Council of Science Editors:

Liu J. Further Studies in Adenosinergic and Monoaminergic Mechanisms of Analgesia by Amitriptyline. [Masters Thesis]. Dalhousie University; 2012. Available from: http://hdl.handle.net/10222/15329

University of Cambridge

4. Thomas, Jennifer Ann. Engineering the angiotensin II type 1 receptor for structural studies.

Degree: PhD, 2015, University of Cambridge

URL: https://doi.org/10.17863/CAM.15945 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.649397

► G protein-coupled receptors (GPCRs) are eukaryotic integral membrane proteins that perform transmembrane signal transduction. Due to their pivotal role in a wide range of essential… (more)

▼ G protein-coupled receptors (GPCRs) are eukaryotic integral membrane proteins that perform transmembrane signal transduction. Due to their pivotal role in a wide range of essential physiological functions GPCRs represent a high proportion of all drug targets. High resolution X-ray structures of GPCRs are however underrepresented in the Protein Data Bank. This is due to their instability in detergent, low expression levels and the presence of misfolded receptors in many heterologous expression systems. The objective of this project was to engineer the angiotensin II type 1 receptor (AT1R), a human GPCR, to make it suitable for structural studies. It was determined that detergentsolubilised AT1R was thermostable with antagonist bound with an apparent Tm of ~45°C, which was sufficiently stable for purification without further thermostabilisation by rational mutagenesis. Two expression systems were then evaluated for large-scale production of AT1R, namely baculovirus-mediated expression in insect cells and mammalian expression in HEK293 cells. Radioligand binding assays showed that only the mammalian system produced sufficient quantities of active AT1R for structural studies. Expression in the mammalian system was further optimised to approximately 6 mg/L. An AT1R-GFP fusion was created to examine membrane localisation using confocal laser scanning microscopy, to assay expression levels, to select highly expressing monoclonal cell lines using fluorescence activated flow cytometry and to develop a fluorescence size-exclusion chromatographybased assay to examine the suitability of 12 different ligands for co-crystallization. AT1R was also engineered to facilitate crystallisation, including C-terminal truncations to remove predicted disordered regions and bacteriophage T4-lysozyme being added to the third intracellular loop to provide additional points of contact for crystallisation, which increased the apparent Tm by approximately 10°C. All modified versions of AT1R were assessed for expression, stability and monodispersity. Additionally a rapid western blotting based assay was developed for the detection of unfolded membrane proteins, which will have wide applicability in the field.

Subjects/Keywords: 572; G protein coupled receptors; GPCR; angiotensin II receptor; eukaryotic membrane protein expression; GFP; FSEC; protean agonism; fluorescence-detection size-exclusion chromatography; adenosine A1 receptor

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Thomas, J. A. (2015). Engineering the angiotensin II type 1 receptor for structural studies. (Doctoral Dissertation). University of Cambridge. Retrieved from https://doi.org/10.17863/CAM.15945 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.649397

Chicago Manual of Style (16^th Edition):

Thomas, Jennifer Ann. “Engineering the angiotensin II type 1 receptor for structural studies.” 2015. Doctoral Dissertation, University of Cambridge. Accessed February 25, 2021. https://doi.org/10.17863/CAM.15945 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.649397.

MLA Handbook (7^th Edition):

Thomas, Jennifer Ann. “Engineering the angiotensin II type 1 receptor for structural studies.” 2015. Web. 25 Feb 2021.

Vancouver:

Thomas JA. Engineering the angiotensin II type 1 receptor for structural studies. [Internet] [Doctoral dissertation]. University of Cambridge; 2015. [cited 2021 Feb 25]. Available from: https://doi.org/10.17863/CAM.15945 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.649397.

Council of Science Editors:

Thomas JA. Engineering the angiotensin II type 1 receptor for structural studies. [Doctoral Dissertation]. University of Cambridge; 2015. Available from: https://doi.org/10.17863/CAM.15945 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.649397

University of Cambridge

5. Thomas, Jennifer Ann. Engineering the angiotensin II type 1 receptor for structural studies.

Degree: PhD, 2015, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/247919https://www.repository.cam.ac.uk/bitstream/1810/247919/2/license.txt ; https://www.repository.cam.ac.uk/bitstream/1810/247919/3/license_rdf ; https://www.repository.cam.ac.uk/bitstream/1810/247919/6/J_Thomas_Final%20_Thesis.pdf.txt ; https://www.repository.cam.ac.uk/bitstream/1810/247919/7/J_Thomas_Final%20_Thesis.pdf.jpg

► G protein-coupled receptors (GPCRs) are eukaryotic integral membrane proteins that perform transmembrane signal transduction. Due to their pivotal role in a wide range of essential… (more)

▼ G protein-coupled receptors (GPCRs) are eukaryotic integral membrane proteins that perform transmembrane signal transduction. Due to their pivotal role in a wide range of essential physiological functions GPCRs represent a high proportion of all drug targets. High resolution X-ray structures of GPCRs are however underrepresented in the Protein Data Bank. This is due to their instability in detergent, low expression levels and the presence of misfolded receptors in many heterologous expression systems. The objective of this project was to engineer the angiotensin II type 1 receptor (AT1R), a human GPCR, to make it suitable for structural studies. It was determined that detergentsolubilised AT1R was thermostable with antagonist bound with an apparent Tm of ~45°C, which was sufficiently stable for purification without further thermostabilisation by rational mutagenesis. Two expression systems were then evaluated for large-scale production of AT1R, namely baculovirus-mediated expression in insect cells and mammalian expression in HEK293 cells. Radioligand binding assays showed that only the mammalian system produced sufficient quantities of active AT1R for structural studies. Expression in the mammalian system was further optimised to approximately 6 mg/L. An AT1R-GFP fusion was created to examine membrane localisation using confocal laser scanning microscopy, to assay expression levels, to select highly expressing monoclonal cell lines using fluorescence activated flow cytometry and to develop a fluorescence size-exclusion chromatographybased assay to examine the suitability of 12 different ligands for co-crystallization. AT1R was also engineered to facilitate crystallisation, including C-terminal truncations to remove predicted disordered regions and bacteriophage T4-lysozyme being added to the third intracellular loop to provide additional points of contact for crystallisation, which increased the apparent Tm by approximately 10°C. All modified versions of AT1R were assessed for expression, stability and monodispersity. Additionally a rapid western blotting based assay was developed for the detection of unfolded membrane proteins, which will have wide applicability in the field.

Subjects/Keywords: G protein coupled receptors; GPCR; angiotensin II receptor; eukaryotic membrane protein expression; GFP; FSEC; protean agonism; fluorescence-detection size-exclusion chromatography; adenosine A1 receptor

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Thomas, J. A. (2015). Engineering the angiotensin II type 1 receptor for structural studies. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/247919https://www.repository.cam.ac.uk/bitstream/1810/247919/2/license.txt ; https://www.repository.cam.ac.uk/bitstream/1810/247919/3/license_rdf ; https://www.repository.cam.ac.uk/bitstream/1810/247919/6/J_Thomas_Final%20_Thesis.pdf.txt ; https://www.repository.cam.ac.uk/bitstream/1810/247919/7/J_Thomas_Final%20_Thesis.pdf.jpg

Chicago Manual of Style (16^th Edition):

Thomas, Jennifer Ann. “Engineering the angiotensin II type 1 receptor for structural studies.” 2015. Doctoral Dissertation, University of Cambridge. Accessed February 25, 2021. https://www.repository.cam.ac.uk/handle/1810/247919https://www.repository.cam.ac.uk/bitstream/1810/247919/2/license.txt ; https://www.repository.cam.ac.uk/bitstream/1810/247919/3/license_rdf ; https://www.repository.cam.ac.uk/bitstream/1810/247919/6/J_Thomas_Final%20_Thesis.pdf.txt ; https://www.repository.cam.ac.uk/bitstream/1810/247919/7/J_Thomas_Final%20_Thesis.pdf.jpg.

MLA Handbook (7^th Edition):

Thomas, Jennifer Ann. “Engineering the angiotensin II type 1 receptor for structural studies.” 2015. Web. 25 Feb 2021.

Vancouver:

Thomas JA. Engineering the angiotensin II type 1 receptor for structural studies. [Internet] [Doctoral dissertation]. University of Cambridge; 2015. [cited 2021 Feb 25]. Available from: https://www.repository.cam.ac.uk/handle/1810/247919https://www.repository.cam.ac.uk/bitstream/1810/247919/2/license.txt ; https://www.repository.cam.ac.uk/bitstream/1810/247919/3/license_rdf ; https://www.repository.cam.ac.uk/bitstream/1810/247919/6/J_Thomas_Final%20_Thesis.pdf.txt ; https://www.repository.cam.ac.uk/bitstream/1810/247919/7/J_Thomas_Final%20_Thesis.pdf.jpg.

Council of Science Editors:

Thomas JA. Engineering the angiotensin II type 1 receptor for structural studies. [Doctoral Dissertation]. University of Cambridge; 2015. Available from: https://www.repository.cam.ac.uk/handle/1810/247919https://www.repository.cam.ac.uk/bitstream/1810/247919/2/license.txt ; https://www.repository.cam.ac.uk/bitstream/1810/247919/3/license_rdf ; https://www.repository.cam.ac.uk/bitstream/1810/247919/6/J_Thomas_Final%20_Thesis.pdf.txt ; https://www.repository.cam.ac.uk/bitstream/1810/247919/7/J_Thomas_Final%20_Thesis.pdf.jpg

6. Pinto, Isa Eunice Costa Figueiredo Paula. The role of cGMP on adenosine A1 receptor-mediated inhibition of synaptic transmission at the hippocampus.

Degree: 2014, RCAAP

URL: https://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/5663

►

The adenosine A1 receptor is highly expressed in hippocampus where it inhibits synaptic transmission and has neuroprotective activity. Similar actions are obtained by increasing the… (more)

▼

The adenosine A1 receptor is highly expressed in hippocampus where it inhibits synaptic transmission and has neuroprotective activity. Similar actions are obtained by increasing the concentration of the second messenger cGMP and recently it was found that activation of adenosine A1 receptor increased cGMP levels in the nervous system, but the role of cGMP on adenosine A1 receptor mediated inhibition of synaptic transmission remains to be established. This work addressed if the adenosine A1 receptor inhibitory effect on neurotransmission is dependent on the cGMP pathway. To answer this question investigated in what extent increasing the levels of cGMP (with a phosphodiesterases inhibitor and a cGMP analog), or blocking the cGMP pathway (using nitric oxide synthase, protein kinase G and soluble guanylyl cyclase inhibitors) modify the inhibitory effect of an A1 receptor agonist on synaptic transmission. The hippocampal slice was used as an experimental model and neurotransmission evaluated through extracelular electrophysiological recording technique, specifically by measuring the slope of field excitatory postsynaptic potentials (fEPSPs) evoked by electrical stimulation. N6-cyclopentyladenosine (CPA, 15nM), a selective adenosine A1 receptor agonist, reversibly decreased the fEPSPs by 48% ± 2.1% (n=5; P<0.05). Incubation of the slices with a phosphodiesterase inhibitor Bay 60-7550 (100 nM), in order to prevent cGMP degradation, did not modify the CPA (15 nM) inhibitory effect on fEPSPs (50%±2.8%, n=5; P>0.05 when compared with CPA alone). The presence of a membrane-permeable analog of cGMP, 8-pCPTP-cGMP (10 µM), also did not significantly affect (P>0.05) the CPA (15nM) inhibitory effect on fEPSPs (59.0%±4.5% in the absence and 50%±8.6% in the presence of 8-pCTP-cGMP, n=4). On the other hand, inhibition of nitric oxide synthase (NOS) by L-NAME (200 µM) decreased (P<0.05) the CPA (15nM) inhibitory effect on fEPSPs (54%±5.3% in the absence and 23%±5.7% in the presence of L-NAME, n=5, female rats). In male rats, the presence of a Protein Kinase G (PKG) inhibitor (KT5823, 1nM) decreased the inhibitory effect of CPA (15nM) on fEPSPs by 45.0%±8.9% (n=4, P<0.05 compared with zero); similar results were obtained in females. Finally the effect of an inhibitor of soluble guanylyl cyclase (sGC), ODQ (10 µM), on the CPA (15 nM) inhibitory action on fEPSPs was investigated. In males ODQ decreased (P<0.05) the CPA inhibitory effect (50%±4.3% in the absence and 39%±6.0% in the presence of ODQ, n=4), but only when adenosine deaminase (1 U/ml) was present; similar results were found in females. In conclusion, the results strongly suggest that inhibitory action of adenosine A1 receptors on glutamatergic neurotransmission at the hippocampus is, at least partially, mediated by activation of the NOS/sGC/cGMP/PKG pathway.

A adenosina é libertada para o meio extracelular em situação de actividade neuronal prolongada ou após insulto neurotóxico. A adenosina, via activação do receptor A1, inibe a transmissão sináptica e previne o dano…

Advisors/Committee Members: Cascalheira, José Francisco da Silva, Sebastião, Ana.

Subjects/Keywords: Adenosine A1 Receptor; Cgmp; Hippocampus; Phosphodiesterase; Protein Kinase G; Soluble Guanylyl Cyclase; Synaptic Transmission; Domínio/Área Científica::Engenharia e Tecnologia::Engenharia Química

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Pinto, I. E. C. F. P. (2014). The role of cGMP on adenosine A1 receptor-mediated inhibition of synaptic transmission at the hippocampus. (Thesis). RCAAP. Retrieved from https://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/5663

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Pinto, Isa Eunice Costa Figueiredo Paula. “The role of cGMP on adenosine A1 receptor-mediated inhibition of synaptic transmission at the hippocampus.” 2014. Thesis, RCAAP. Accessed February 25, 2021. https://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/5663.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Pinto, Isa Eunice Costa Figueiredo Paula. “The role of cGMP on adenosine A1 receptor-mediated inhibition of synaptic transmission at the hippocampus.” 2014. Web. 25 Feb 2021.

Vancouver:

Pinto IECFP. The role of cGMP on adenosine A1 receptor-mediated inhibition of synaptic transmission at the hippocampus. [Internet] [Thesis]. RCAAP; 2014. [cited 2021 Feb 25]. Available from: https://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/5663.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Pinto IECFP. The role of cGMP on adenosine A1 receptor-mediated inhibition of synaptic transmission at the hippocampus. [Thesis]. RCAAP; 2014. Available from: https://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/5663

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

7. Klaasse, Elisabeth Cornelia. Non-ribose ligands for the human adenosine A1 receptor.

Degree: 2008, Medicinal Chemistry, LACDR, Faculty of Science, Leiden University

URL: http://hdl.handle.net/1887/12936

► This thesis describes new, non-ribose ligands for the human Adenosine A1 Receptor (hA1R). An introduction to the four adenosine receptors subtypes, their history and cloning,… (more)

Subjects/Keywords: Activity; Affinity; Allosteric modulation; Human Adenosine A1 Receptor; Internalization; Non-ribose ligands; Activity; Affinity; Allosteric modulation; Human Adenosine A1 Receptor; Internalization; Non-ribose ligands

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Klaasse, E. C. (2008). Non-ribose ligands for the human adenosine A1 receptor. (Doctoral Dissertation). Medicinal Chemistry, LACDR, Faculty of Science, Leiden University. Retrieved from http://hdl.handle.net/1887/12936

Chicago Manual of Style (16^th Edition):

Klaasse, Elisabeth Cornelia. “Non-ribose ligands for the human adenosine A1 receptor.” 2008. Doctoral Dissertation, Medicinal Chemistry, LACDR, Faculty of Science, Leiden University. Accessed February 25, 2021. http://hdl.handle.net/1887/12936.

MLA Handbook (7^th Edition):

Klaasse, Elisabeth Cornelia. “Non-ribose ligands for the human adenosine A1 receptor.” 2008. Web. 25 Feb 2021.

Vancouver:

Klaasse EC. Non-ribose ligands for the human adenosine A1 receptor. [Internet] [Doctoral dissertation]. Medicinal Chemistry, LACDR, Faculty of Science, Leiden University; 2008. [cited 2021 Feb 25]. Available from: http://hdl.handle.net/1887/12936.

Council of Science Editors:

Klaasse EC. Non-ribose ligands for the human adenosine A1 receptor. [Doctoral Dissertation]. Medicinal Chemistry, LACDR, Faculty of Science, Leiden University; 2008. Available from: http://hdl.handle.net/1887/12936

University of Otago

8. Singh, Sameek. Development of fluorescent ligands for A1 adenosine receptor and cannabinoid receptors .

Degree: University of Otago

URL: http://hdl.handle.net/10523/8457

► Adenosine A1 receptor (A1AR), cannabinoid type 1 receptor (CB1R) and cannabinoid type 2 receptor (CB2R) are class A G protein-coupled receptors (GPCRs) and play important… (more)

▼ Adenosine A1 receptor (A1AR), cannabinoid type 1 receptor (CB1R) and cannabinoid type 2 receptor (CB2R) are class A G protein-coupled receptors (GPCRs) and play important roles in human pathophysiological conditions such as cardiovascular, neurological, metabolic and immunological disorders. Fluorescent ligands are powerful tools to investigate processes such as receptor expression, localisation, trafficking and receptor-protein interactions in the native cell environment. Fluorescent ligands can also be used as tracers in pharmacological assays, instead of the commonly used radioligands that carry inherent safety risks. The development of fluorescent ligands with high affinity, selectivity and suitable imaging properties for A1AR, CB1R and CB2R would greatly contribute to an increased understanding of receptor biology and thus facilitate the drug development process. Development of fluorescent ligands with sufficient polarity for cannabinoid receptors (CBRs), which have lipid-based endogenous ligands, is an especially challenging task. This thesis describes the development of small molecule-based fluorescent ligands for A1AR, CB1R and CB2R, via attachment of a linker and fluorophore to a ligand. (Benzimidazolyl)isoquinolinols, analogues of previously reported high affinity A1AR (benzimidazolyl)isoquinolines, were explored in chapter 2 for the development of A1AR fluorescent ligands. A procedure for 2,3-dichloro-5,6-dicyano-1,4-benzoquinone (DDQ) mediated aromatisation of tetrahydroisoquinolines and multistep synthesis for the preparation of (benzimidazolyl)isoquinolinols was developed. Based on the previously reported structure–activity relationship (SAR), linkers (and linker plus fluorophore conjugates) were introduced in the C-6 or C-7 position of (benzimidazolyl)isoquinolinols. Unfortunately, these fluorescent ligands did not exhibit any significant affinity for A1AR in a bioluminescence resonance energy transfer (BRET) assay using the NanoLuc luciferase and it was concluded that (benzimidazolyl)isoquinolinols might not be a suitable scaffold for the development of A1AR fluorescent ligands. NMR spectroscopy and reverse phase HPLC studies showed (benzimidazolyl)isoquinolinols exhibit tautomerism. Chromenopyrazoles, previously reported as high affinity CB1R ligands, were investigated for development into CB1R fluorescent ligands in chapter 3. Based on previous SAR, linkers then fluorophores were introduced at six different chromenopyrazole positions. Disappointingly, fluorescent chromenopyrazoles did not exhibit high affinity for CB1R in a radioligand binding assay. However, several chromenopyrazoles including a linker conjugate 3.22 and a peptide linker conjugate 3.39 exhibited high affinity for CB2R that were promising candidates for development of CB2R fluorescent ligands. All of the chromenopyrazoles that were evaluated in a cyclic adenosine monophosphate (cAMP) functional assay behaved as agonists at CB2R. Docking studies were carried out using a CB2R homology model and showed that high affinity CB2R… Advisors/Committee Members: Vernall, Andrea (advisor).

Subjects/Keywords: Adenosine A1 receptor; Cannabinoid type 1 receptor; Cannabinoid type 2 receptor; GPCRs; Chemical tools; Fluorescent ligands

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APA (6^th Edition):

Singh, S. (n.d.). Development of fluorescent ligands for A1 adenosine receptor and cannabinoid receptors . (Doctoral Dissertation). University of Otago. Retrieved from http://hdl.handle.net/10523/8457

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Chicago Manual of Style (16^th Edition):

Singh, Sameek. “Development of fluorescent ligands for A1 adenosine receptor and cannabinoid receptors .” Doctoral Dissertation, University of Otago. Accessed February 25, 2021. http://hdl.handle.net/10523/8457.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

MLA Handbook (7^th Edition):

Singh, Sameek. “Development of fluorescent ligands for A1 adenosine receptor and cannabinoid receptors .” Web. 25 Feb 2021.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

Singh S. Development of fluorescent ligands for A1 adenosine receptor and cannabinoid receptors . [Internet] [Doctoral dissertation]. University of Otago; [cited 2021 Feb 25]. Available from: http://hdl.handle.net/10523/8457.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Council of Science Editors:

Singh S. Development of fluorescent ligands for A1 adenosine receptor and cannabinoid receptors . [Doctoral Dissertation]. University of Otago; Available from: http://hdl.handle.net/10523/8457

Note: this citation may be lacking information needed for this citation format:
No year of publication.

9. Katz, Natalie. Modulation of Nociception in Painful Diabetic Neuropathy.

Degree: PhD, Neurosciences, 2014, University of Kansas

URL: http://hdl.handle.net/1808/14503

► Diabetes mellitus has become a global pandemic, with almost 350 million individuals world-wide affected by the disease. There are two common forms, characterized by either… (more)

▼ Diabetes mellitus has become a global pandemic, with almost 350 million individuals world-wide affected by the disease. There are two common forms, characterized by either a lack of insulin production or peripheral insulin resistance. Diabetic peripheral neuropathy is the most common and debilitating complication in both forms, and approximately 30% of individuals with diabetic neuropathy will experience pain that significantly impacts their quality of life. Unfortunately, symptomatic treatment modalities are often ineffective and carry significant risk of systemic adverse effects. The work contained herein used a rodent model of painful diabetic neuropathy following induction of diabetes with the pancreatic beta cell toxin, streptozocin (STZ). Results show that diabetes reduces the ability of specialized enzymes, termed ectonucleotidases, to hydrolyze extracellular AMP into the analgesic small molecule adenosine. At this same time, diabetic mice displayed significant mechanical allodynia, suggesting that altered adenosine production and decreased activation of the antinociceptive A1 adenosine receptor (A1R) may contribute to the development of painful diabetic neuropathy. In the dorsal horn of the spinal cord, A1R is highly expressed where peripheral pain sensing neurons terminate, placing it in prime location to modulate nociceptive signaling. Central delivery of A1R agonists, such as AMP, adenosine and the specific A1R agonist, N6-cyclopentyladenosine (CPA), significantly improved mechanical withdrawal thresholds in diabetic mice to levels that were not significantly different from nondiabetic mice. A1R is a G-protein coupled receptor whose activation results in initiation of downstream second messenger systems. Inhibition of cAMP production and robust activation of Akt were observed following central delivery of adenosine and CPA, suggesting these pathways contribute to the antiallodynic effects of activation of A1R. Central delivery of A1R agonists is not ideal for translation to the human population. Accordingly, peripheral delivery methods were evaluated to determine the efficacy of this therapeutic intervention in painful diabetic neuropathy. Surprisingly, peripheral delivery of CPA resulted in significant improvement in mechanical allodynia in diabetic mice, confirming that the A1R-mediated antinociceptive pathway is accessible from the periphery. These observations warrant further investigation into this endogenous antinociceptive pathway for the development of novel therapeutic treatment options for individuals suffering from painful diabetic neuropathy. Advisors/Committee Members: Wright, Douglas E. (advisor), Berman, Nancy E. J. (cmtemember), Christianson, Julie A. (cmtemember), McCarson, Kenneth E. (cmtemember), Robbins, David E. (cmtemember).

Subjects/Keywords: Neurosciences; Biology; Adenosine; Adenosine a1 receptor; Diabetes; Mechanical allodynia; Pain; Peripheral neuropathy

…downstream of A 1 R 30 Figure 4 Ectonucleotidase-mediated metabolism of ATP into adenosine 36… …cultures is increased in diabetic mice, and is restored by overnight incubation adenosine… …form of insulin, and binds to and activates a G-protein couple receptor (GPCR) that… …tramadol, a weak µ-opioid receptor agonist, and controlled release oxycodone, a strong µ-opioid… …receptor agonist, have been shown to be successful in reducing pain. Caution is advised when…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Katz, N. (2014). Modulation of Nociception in Painful Diabetic Neuropathy. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/14503

Chicago Manual of Style (16^th Edition):

Katz, Natalie. “Modulation of Nociception in Painful Diabetic Neuropathy.” 2014. Doctoral Dissertation, University of Kansas. Accessed February 25, 2021. http://hdl.handle.net/1808/14503.

MLA Handbook (7^th Edition):

Katz, Natalie. “Modulation of Nociception in Painful Diabetic Neuropathy.” 2014. Web. 25 Feb 2021.

Vancouver:

Katz N. Modulation of Nociception in Painful Diabetic Neuropathy. [Internet] [Doctoral dissertation]. University of Kansas; 2014. [cited 2021 Feb 25]. Available from: http://hdl.handle.net/1808/14503.

Council of Science Editors:

Katz N. Modulation of Nociception in Painful Diabetic Neuropathy. [Doctoral Dissertation]. University of Kansas; 2014. Available from: http://hdl.handle.net/1808/14503

University of Houston

10. Gu, Feng 1978-. Controlling Febrile Seizures in a Model of Dravet Syndrome.

Degree: PhD, Biology, University of Houston

URL: http://hdl.handle.net/10657/3402

► Severe myoclonic epilepsy of infancy (SMEI) or Dravet syndrome is one of the most devastating types of childhood epilepsies. Children with SMEI suffer from febrile… (more)

▼ Severe myoclonic epilepsy of infancy (SMEI) or Dravet syndrome is one of the most devastating types of childhood epilepsies. Children with SMEI suffer from febrile and afebrile seizures (FS and aFS), ataxia, and social and cognitive dysfunctions. SMEI is pharmacologically intractable and can be fatal in 10-20% of patients. 70%-80% of SMEI patients are found to have SCN1A gene mutations. Recent studies of mouse models of SMEI (mSMEI) with SCN1A gene mutations have elucidated molecular and cellular mechanisms that may account for the epileptogenesis. There remains, however, a critical need to further elucidate how SCN1A gene mutation impacts neuronal activity in key anatomical circuits, and to develop new strategies for controlling seizures in SMEI. This dissertation aims to analyze and control neural circuit excitability and hyperthermia-induced FS both in vitro and in vivo using mSMEI carrying a SCN1A gene mutation. Using a combination of electrophysiology and fast voltage-sensitive dye imaging (VSDI) we studied synaptic excitatory/inhibitory balance, characteristics of neural activity propagation, and hyperthermia-induced FS-like events (FSLEs) in the hippocampus of mSMEI in vitro. Our in vitro studies reveal significant excitation and inhibition (E/I) imbalance in mSMEI, showing decreased inhibition, increased excitation, evoked neural activity that is abnormally wide-spread, and a decrease in FSLE threshold in the hippocampal circuits. To control hyperthermia-induced hyperexcitability and seizure activity (also referred to as febrile seizures), we used adenosine A1 receptor (AIR) agonist N6-cyclopentyladenosine (CPA). We found that in vitro, low concentration (50nM) of CPA significantly reduced hippocampal circuit hyperexcitability and blocked hyperthermia-induced FSLEs without blocking excitatory synaptic transmission. Furthermore, we tested whether CPA would have an equivalent effect on hyperthermia-induced FS in vivo. We found that SMEI transgenic animals had significantly lower FS threshold than their wild-type littermates. Acute injection of CPA prior to hyperthermia exposure effectively suppressed FS. In addition to the acute effect of CPA, we also tested if chronic treatment of SMEI mice with CPA during early postnatal development (postnatal days P11-20) can have a long-lasting anti-convulsant effect. We discovered that 24 hours and even 10 days after the last drug treatment (at P20), FS threshold in vivo was still significantly reduced. Our follow-up studies in vitro, following the chronic treatment in vivo, showed that following 10 days of treatment, synaptic excitation was decreased while the inhibitory responses were unaltered. Our findings suggest that A1R agonist CPA may serve as an effective compound to recover the E/I balance and control or prevent epileptogenesis in SMEI. Advisors/Committee Members: Ziburkus, Jokubas (advisor), Dauwalder, Brigitte (committee member), Leasure, J. Leigh (committee member), Rea, Michael A. (committee member).

Subjects/Keywords: Epilepsy; Dravet syndrome; Seizure; SCN1A gene; Hyperthermia; Hippocampal Circuit; Hippocampus; Optical Imaging; Excitation/Inhibition balance; Adenosine A1 receptor

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Gu, F. 1. (n.d.). Controlling Febrile Seizures in a Model of Dravet Syndrome. (Doctoral Dissertation). University of Houston. Retrieved from http://hdl.handle.net/10657/3402

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Chicago Manual of Style (16^th Edition):

Gu, Feng 1978-. “Controlling Febrile Seizures in a Model of Dravet Syndrome.” Doctoral Dissertation, University of Houston. Accessed February 25, 2021. http://hdl.handle.net/10657/3402.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

MLA Handbook (7^th Edition):

Gu, Feng 1978-. “Controlling Febrile Seizures in a Model of Dravet Syndrome.” Web. 25 Feb 2021.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

Gu F1. Controlling Febrile Seizures in a Model of Dravet Syndrome. [Internet] [Doctoral dissertation]. University of Houston; [cited 2021 Feb 25]. Available from: http://hdl.handle.net/10657/3402.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Council of Science Editors:

Gu F1. Controlling Febrile Seizures in a Model of Dravet Syndrome. [Doctoral Dissertation]. University of Houston; Available from: http://hdl.handle.net/10657/3402

Note: this citation may be lacking information needed for this citation format:
No year of publication.

11. Tikh, Eugene I. Regulation of Contractility by Adenosine A₁ and A_2A Receptors in the Murine Heart: Role of Protein Phosphatase 2A: A Dissertation.

Degree: PhD, Microbiology and Physiological Systems, 2006, U of Massachusetts : Med

URL: https://escholarship.umassmed.edu/gsbs_diss/130

► Adenosine is a nucleoside that plays an important role in the regulation of contractility in the heart. Adenosine receptors are G-protein coupled and those… (more)

Subjects/Keywords: Myocardial Contraction; Receptor; Adenosine A1; Receptor; Adenosine A2A; Adenosine; Phosphoprotein Phosphatase; Heart; Mice; Amino Acids, Peptides, and Proteins; Animal Experimentation and Research; Cardiovascular System; Circulatory and Respiratory Physiology; Heterocyclic Compounds; Musculoskeletal, Neural, and Ocular Physiology; Nucleic Acids, Nucleotides, and Nucleosides; Physiology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Tikh, E. I. (2006). Regulation of Contractility by Adenosine A₁ and A_2A Receptors in the Murine Heart: Role of Protein Phosphatase 2A: A Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from https://escholarship.umassmed.edu/gsbs_diss/130

Chicago Manual of Style (16^th Edition):

Tikh, Eugene I. “Regulation of Contractility by Adenosine A₁ and A_2A Receptors in the Murine Heart: Role of Protein Phosphatase 2A: A Dissertation.” 2006. Doctoral Dissertation, U of Massachusetts : Med. Accessed February 25, 2021. https://escholarship.umassmed.edu/gsbs_diss/130.

MLA Handbook (7^th Edition):

Tikh, Eugene I. “Regulation of Contractility by Adenosine A₁ and A_2A Receptors in the Murine Heart: Role of Protein Phosphatase 2A: A Dissertation.” 2006. Web. 25 Feb 2021.

Vancouver:

Tikh EI. Regulation of Contractility by Adenosine A₁ and A_2A Receptors in the Murine Heart: Role of Protein Phosphatase 2A: A Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2006. [cited 2021 Feb 25]. Available from: https://escholarship.umassmed.edu/gsbs_diss/130.

Council of Science Editors:

Tikh EI. Regulation of Contractility by Adenosine A₁ and A_2A Receptors in the Murine Heart: Role of Protein Phosphatase 2A: A Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 2006. Available from: https://escholarship.umassmed.edu/gsbs_diss/130

12. Klaft, Zin-Juan. Blockierung von Carbamazepin-resistenter epileptiformer Aktivität durch Aktivierung von Adenosin A1 Rezeptoren in humanen neokortikalen Hirnschnitten von pharmakoresistenten Epilepsiepatienten.

Degree: 2017, Freie Universität Berlin

URL: http://dx.doi.org/10.17169/refubium-5205

► Einleitung: Resistenz gegenüber antiepileptischer Medikation ist ein bedeutendes klinisches Problem und betrifft circa 30 % aller Epilepsiepatienten und bis zu 80 % der Patienten mit… (more)

▼ Einleitung: Resistenz gegenüber antiepileptischer Medikation ist ein bedeutendes klinisches Problem und betrifft circa 30 % aller Epilepsiepatienten und bis zu 80 % der Patienten mit Temporallappen-Epilepsie. Die chirurgische Resektion der iktogenen Hirnstrukturen ist nur für eine kleine Minderheit der pharmakoresistenten Patienten möglich. Daher ist die Entwicklung von neuen pharmakologischen Behandlungen ein wichtiger Gegenstand der neurologischen Forschung. Das purinerge Rezeptorsystem besteht aus Adenosinrezeptoren und P2-Rezeptoren, welche durch Adenosintriphosphat (ATP) aktiviert werden. Purinerge Rezeptoren modulieren die synaptische Transmission und werden daher als potenzielle Zielstrukturen für die Entwicklung neuer antikonvulsiver Medikamente gesehen. Die vorliegende in vitro Studie untersucht die purinerge Modulation von induzierter epileptiformer Aktivität in humanen neokortikalen Hirnschnitten. Methodik: Insgesamt wurden 77 neokortikale Hirnschnitte von 17 Patienten mit epilepsiechirurgischen Eingriffen zwischen den Jahren 2010 und 2015 untersucht. Lokale Feldpotenzial Ableitungen wurden in den Schichten V/VI des humanen Neokortex durchgeführt. Um stabile epileptiforme Aktivität, sogenannte anfallsartige Ereignisse (AAE), auszulösen, wurde in der artifiziellen cerebrospinalen Flüssigkeit (aCSF) die extrazelluläre Kalium-Konzentration auf 8 mM erhöht und dem aCSF 50 µM des GABAA Rezeptorantagonisten Bicucullin-Methiodid hinzugefügt. Ergebnisse: 1 µM des selektiven A1 Rezeptoragonisten SDZ WAG 994 blockierte AAEs vollständig in 73 % der Hirnschnitte. Dies entspricht einem signifikant größeren Anteil an Hirnschnitten mit unterdrückten AAEs als durch Applikation von 300 µM ATP (18 %) oder 300 µM Adenosin (13 %) beobachtet wurde. Auch der antikonvulsive Effekt der physiologischen purinergen Breitbandagonisten Adenosin und ATP wurde am ehesten durch Aktivierung der A1 Rezeptoren ausgelöst. Des Weiteren wurden durch Applikation des selektiven A1 Rezeptoragonisten in 71 % der Hirnschnitte auch die AAEs unterdrückt, die resistent gegenüber der Applikation von 50 µM Carbamazepin (CBZ) waren. Bei Applikation selektiver P2Y1, P2X1, P2X3, P2X2/3 und P2X7 Rezeptorantagonisten wurde keine relevante Modulation der AAE Parameter beobachtet, sodass eine mögliche Beteiligung endogen aktivierter P2 Rezeptoren unwahrscheinlich ist. Schlussfolgerung: Das wichtigste Ergebnis der vorliegenden Arbeit ist die überraschend effiziente Unterdrückung CBZ-resistenter epileptiformer Aktivität in humanen neokortikalen Hirnschnitten durch den selektiven A1 Rezeptoragonisten SDZ WAG 994. Diese Studie bestätigt die bekannte antikonvulsive Wirkung von Adenosin und beschreibt des Weiteren erstmals die effiziente Blockierung von epileptiformer Aktivität durch direkte A1 Rezeptoraktivierung in humanen neokortikalen Hirnschnitten. Interessanterweise ist bekannt, dass die Gabe von SDZ WAG 994 durch den Menschen toleriert wird. Dessen Anwendung könnte daher einen neuartigen pharmakologischen Ansatz zur Therapie von Anfallserkrankungen… Advisors/Committee Members: m (gender), N.N. (firstReferee), N.N. (furtherReferee).

Subjects/Keywords: epilepsy; status epilepticus; adenosine; A1 receptor agonist; human brain slices; electrophysiology; pharmacoresistance; purines; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit

…Heinemann U. Adenosine A1 receptor-mediated suppression of carbamazepine-resistant seizure-like… …NEUROBIOLOGY 68 CURRENT OPINION IN 4,784 4.469 0.011510 NEUROLOGY 9 Publikation Adenosine A1… …Adenosine A 1 receptor-mediated suppression of carbamazepine-resistant seizure-like events in… …Extracellular ATP differentially affects epileptiform activity via P2X7 and adenosine A1 receptors in… …receptor-mediated suppression of carbamazepine-resistant seizure-like events in neocortical…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Klaft, Z. (2017). Blockierung von Carbamazepin-resistenter epileptiformer Aktivität durch Aktivierung von Adenosin A1 Rezeptoren in humanen neokortikalen Hirnschnitten von pharmakoresistenten Epilepsiepatienten. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-5205

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Klaft, Zin-Juan. “Blockierung von Carbamazepin-resistenter epileptiformer Aktivität durch Aktivierung von Adenosin A1 Rezeptoren in humanen neokortikalen Hirnschnitten von pharmakoresistenten Epilepsiepatienten.” 2017. Thesis, Freie Universität Berlin. Accessed February 25, 2021. http://dx.doi.org/10.17169/refubium-5205.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Klaft, Zin-Juan. “Blockierung von Carbamazepin-resistenter epileptiformer Aktivität durch Aktivierung von Adenosin A1 Rezeptoren in humanen neokortikalen Hirnschnitten von pharmakoresistenten Epilepsiepatienten.” 2017. Web. 25 Feb 2021.

Vancouver:

Klaft Z. Blockierung von Carbamazepin-resistenter epileptiformer Aktivität durch Aktivierung von Adenosin A1 Rezeptoren in humanen neokortikalen Hirnschnitten von pharmakoresistenten Epilepsiepatienten. [Internet] [Thesis]. Freie Universität Berlin; 2017. [cited 2021 Feb 25]. Available from: http://dx.doi.org/10.17169/refubium-5205.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Klaft Z. Blockierung von Carbamazepin-resistenter epileptiformer Aktivität durch Aktivierung von Adenosin A1 Rezeptoren in humanen neokortikalen Hirnschnitten von pharmakoresistenten Epilepsiepatienten. [Thesis]. Freie Universität Berlin; 2017. Available from: http://dx.doi.org/10.17169/refubium-5205

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

13. Σωτηρίου, Ευάγγελος. Συγκριτική μελέτη της έκφρασης των υπομονάδων του GABAA υποδοχέα και των πρώιμων γονιδίων c-fos και zif-268 σε τομές από τον διαφραγματικό και τον κροταφικό ιππόκαμπο επίμυος πριν καθώς και κατά την διάρκεια της ανάπτυξης των " in vitro " οξέων κυμάτων.

Degree: 2005, University of Patras; Πανεπιστήμιο Πατρών

URL: http://hdl.handle.net/10442/hedi/26839

Subjects/Keywords: Κροταφικός ιππόκαμπος (Κοιλιακός); Διαφραγματικός ιππόκαμπος (Ραχιαίος); γ-ακινοβουτυρικό οξύ και υπότυποι; Επιληψία και συναπτική αναστολή; In vitro οξέα κύματα και ιππόκαμπος; Οξέα κύματα και υπότυποι του γ - αμινοβουτυρικού οξέος; Πρώιμα γονίδια και νευρωνική δραστηριότητα; Α1 υποδοχείς αδενοσίνης και ιππόκαμπος; Temporal hippocampous (Ventral); Septal hippocampus (Dorsal); GABA and subtypes; Epilepsy and synaptic inhibition; In vitro sarp waves and hippocampus; Sarp waves and GABAA receptor sybtypes; Early genes and nevronal activity; A1 adenosine receptors and hippocampus

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Σωτηρίου, . �. (2005). Συγκριτική μελέτη της έκφρασης των υπομονάδων του GABAA υποδοχέα και των πρώιμων γονιδίων c-fos και zif-268 σε τομές από τον διαφραγματικό και τον κροταφικό ιππόκαμπο επίμυος πριν καθώς και κατά την διάρκεια της ανάπτυξης των " in vitro " οξέων κυμάτων. (Thesis). University of Patras; Πανεπιστήμιο Πατρών. Retrieved from http://hdl.handle.net/10442/hedi/26839

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Σωτηρίου, Ευάγγελος. “Συγκριτική μελέτη της έκφρασης των υπομονάδων του GABAA υποδοχέα και των πρώιμων γονιδίων c-fos και zif-268 σε τομές από τον διαφραγματικό και τον κροταφικό ιππόκαμπο επίμυος πριν καθώς και κατά την διάρκεια της ανάπτυξης των " in vitro " οξέων κυμάτων.” 2005. Thesis, University of Patras; Πανεπιστήμιο Πατρών. Accessed February 25, 2021. http://hdl.handle.net/10442/hedi/26839.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Σωτηρίου, Ευάγγελος. “Συγκριτική μελέτη της έκφρασης των υπομονάδων του GABAA υποδοχέα και των πρώιμων γονιδίων c-fos και zif-268 σε τομές από τον διαφραγματικό και τον κροταφικό ιππόκαμπο επίμυος πριν καθώς και κατά την διάρκεια της ανάπτυξης των " in vitro " οξέων κυμάτων.” 2005. Web. 25 Feb 2021.

Vancouver:

Σωτηρίου �. Συγκριτική μελέτη της έκφρασης των υπομονάδων του GABAA υποδοχέα και των πρώιμων γονιδίων c-fos και zif-268 σε τομές από τον διαφραγματικό και τον κροταφικό ιππόκαμπο επίμυος πριν καθώς και κατά την διάρκεια της ανάπτυξης των " in vitro " οξέων κυμάτων. [Internet] [Thesis]. University of Patras; Πανεπιστήμιο Πατρών; 2005. [cited 2021 Feb 25]. Available from: http://hdl.handle.net/10442/hedi/26839.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Σωτηρίου �. Συγκριτική μελέτη της έκφρασης των υπομονάδων του GABAA υποδοχέα και των πρώιμων γονιδίων c-fos και zif-268 σε τομές από τον διαφραγματικό και τον κροταφικό ιππόκαμπο επίμυος πριν καθώς και κατά την διάρκεια της ανάπτυξης των " in vitro " οξέων κυμάτων. [Thesis]. University of Patras; Πανεπιστήμιο Πατρών; 2005. Available from: http://hdl.handle.net/10442/hedi/26839

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

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Open Access Theses and Dissertations