subject:(Chloride Channels physiology 60)

1. Ernest, Nola Jean Sieber. The role of chloride in the volume regulation of human glioma cells.

Degree: PhD, 2007, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,86

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According to the Central Brain Tumor Registry of the United States, the most common primary brain tumors are gliomas, tumors composed of cells of glial… (more)

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According to the Central Brain Tumor Registry of the United States, the most common primary brain tumors are gliomas, tumors composed of cells of glial origin, most commonly astrocytes and oligodendrocytes. The most aggressive of these tumors are characterized by hyperproliferation, marked cellular and nuclear atypia, extensive infiltration into surrounding normal brain tissue, and large areas of cell and tissue death. Previous data published by our lab and others suggest that these biological processes may involve regulated cell volume changes. Using cell volume regulation in the presence of an anisosmotic challenge as a model for cell swelling and shrinkage, cell volume changes have been shown to involve the movement of molecules, or osmolytes, across the plasma membrane through channels and transporters. Water is osmotically obliged to follow the net movement of molecules, resulting in a net flux of water across the plasma membrane and an overall change in cell volume. As the most abundant anion in biological systems, chloride has been shown to be involved in the volume regulation of several cell types. However, chloride-mediated volume changes in human glioma cells have not been extensively studied. It is the primary goal of this dissertation to examine the mechanisms employed by human glioma cells to dynamically regulate their cell volume at rest, in the presence of anisosmotic conditions, and importantly during the biological processes of apoptosis and migration. We confirm the expression of the voltage gated chloride channels ClC-2, 3, and 5 in human glioma cell lines and patient biopsies. In addition, we demonstrate the expression of the cation chloride cotransporters, KCC1, KCC3, and NKCC1. Using a variety of techniques, including electrophysiology, Coulter Counter, and chloride-sensitive fluorescent dyes, we establish that the resting intracellular chloride concentration and cell volume are maintained by the basal activity of chloride cotransporters. While pharmacological inhibition of these cotransporters suggests that they are also involved in cell volume regulation during an aniosomotic challenge, chloride efflux through channels plays a more significant role in post-hyposmotic volume decrease. Similarly, inhibition of chloride channels, but not chloride cation cotransporters, inhibits the cell condensation that occurs in the presence of apoptotic stimuli. Cells treated with chloride channel inhibitors also demonstrated limited caspase 3 activity and DNA fragmentation, suggesting that the volume decrease is necessary for apoptosis. Finally, transwell migration of human glioma cells was blocked in the presence of chloride channel and transport inhibitors, suggesting that the mechanisms involved in cell shrinkage are necessary in glioma cell migration.

xi, 176 p. : ill., digital, PDF file

Neurobiology

Joint Health Sciences

glioma astrocytoma chloride channels migration apoptosis volume regulation

UNRESTRICTED

Advisors/Committee Members: Sontheimer, Harald, Benos, Dale , Brenner, Michael , Guay-Woodford, Lisa , Hablitz, John.

Subjects/Keywords: Brain Neoplasms – physiopathology <; br>; Cell Size <; br>; Chloride Channels – physiology <; br>; Glioma – physiopathology <; br>

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

APA (6^th Edition):

Ernest, N. J. S. (2007). The role of chloride in the volume regulation of human glioma cells. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,86

Chicago Manual of Style (16^th Edition):

Ernest, Nola Jean Sieber. “The role of chloride in the volume regulation of human glioma cells.” 2007. Doctoral Dissertation, University of Alabama – Birmingham. Accessed March 07, 2021. http://contentdm.mhsl.uab.edu/u?/etd,86.

MLA Handbook (7^th Edition):

Ernest, Nola Jean Sieber. “The role of chloride in the volume regulation of human glioma cells.” 2007. Web. 07 Mar 2021.

Vancouver:

Ernest NJS. The role of chloride in the volume regulation of human glioma cells. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2007. [cited 2021 Mar 07]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,86.

Council of Science Editors:

Ernest NJS. The role of chloride in the volume regulation of human glioma cells. [Doctoral Dissertation]. University of Alabama – Birmingham; 2007. Available from: http://contentdm.mhsl.uab.edu/u?/etd,86

2. Habela, Christa Whelan. Progression through the cell cycle is regulated by dynamic chloride dependent changes in cell volumes.

Degree: PhD, 2008, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,444

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The hypothesis that cell volume and the progression of the cell cycle are interdependent has surfaced off and on in the cell cycle literature for… (more)

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The hypothesis that cell volume and the progression of the cell cycle are interdependent has surfaced off and on in the cell cycle literature for the past 30 years. However, a conclusion as to how cell volume is mechanistically involved in cell division has not been reached in mammalian cells. The aim of this dissertation was to establish how volume changes modulate cell cycle progression. Most of the studies addressing this question have examined mass content yet, more recently, focus has been placed on intracellular water, which is determined by the balance between mechanical and osmotic forces. As a result, ion channels and transporters which regulate intracellular osmotic content are integral to the maintenance of cell volume. In this dissertation, I show that a large, rapid and regulated volume decrease occurs as glioma cells progress through mitosis. I refer to this process as pre-mitotic condensation (PMC). This process is functionally linked to DNA condensation prior to cell division as the two events occur simultaneously, and inhibition of PMC results in a prolongation of DNA condensation. Further, my data demonstrates that glioma cells actively accumulate chloride, which acts as the primary energetic driving for cell volume changes in these cells. During the process of PMC, this gradient drives the efflux of chloride through ClC3 channels, which mediates water loss and the volume decrease. Interestingly, chloride accumulation to similar levels can be observed in immature astrocytes and neurons, suggesting that glioma cells recapitulate the biology of immature proliferating cells in the brain. This also suggests that my findings may have broader applicability to cell division in both neural cells and cancer.

xii, 132 p. : ill., digital, PDF file.

Neurobiology

Joint Health Sciences

Voltage Gated Chloride Channels Pre-miotic Condensation DND Condensation C1C3 Mitosis Volume Regulation

UNRESTRICTED

Advisors/Committee Members: Sontheimer, Harald, Bevensee, Mark Engler, Jeffrey Pozzo-Miller, Lucas Theibert, Anne.

Subjects/Keywords: Cell Cycle – physiology<; br>; Cell Movement – physiology<; br>; Cell Proliferation<; br>; Cell Size<; br>; Chloride Channels – physiology<; br>; Chlorides – metabolism<; br>; Cytokinesis – physiology<; br>; Glioma – physiopathology<; br>; Mitosis – physiology<; br>; Neuroglia – physiology

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

APA (6^th Edition):

Habela, C. W. (2008). Progression through the cell cycle is regulated by dynamic chloride dependent changes in cell volumes. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,444

Chicago Manual of Style (16^th Edition):

Habela, Christa Whelan. “Progression through the cell cycle is regulated by dynamic chloride dependent changes in cell volumes.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed March 07, 2021. http://contentdm.mhsl.uab.edu/u?/etd,444.

MLA Handbook (7^th Edition):

Habela, Christa Whelan. “Progression through the cell cycle is regulated by dynamic chloride dependent changes in cell volumes.” 2008. Web. 07 Mar 2021.

Vancouver:

Habela CW. Progression through the cell cycle is regulated by dynamic chloride dependent changes in cell volumes. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2021 Mar 07]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,444.

Council of Science Editors:

Habela CW. Progression through the cell cycle is regulated by dynamic chloride dependent changes in cell volumes. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,444

3. Cuddapah, Vishnu Anand. Regulation Of Clc-3 In Human Malignant Glioma.

Degree: PhD, 2012, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,1394

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Malignant gliomas are the most common and deadly form of primary brain cancer afflicting adults. Current treatment regimens, including surgical debulking, radiotherapy, and chemotherapy, have… (more)

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Malignant gliomas are the most common and deadly form of primary brain cancer afflicting adults. Current treatment regimens, including surgical debulking, radiotherapy, and chemotherapy, have limited efficacy, and median patient survival remains only 14 months. Therefore, novel therapies must target different aspects of glioma biology. Two of the most striking features of this cancer are the unusual ability of glioma cells to robustly proliferate and migrate in the brain, and recent evidence suggests that ClC-3, a voltage-gated Cl- channel/transporter is implicated in both of these processes. We hypothesize that ClC-3 may facilitate proliferation and migration by promoting hydrodynamic shape and volume changes; as Cl- efflux occurs, water osmotically leaves the cytoplasm. These shape and volume changes are critical as, for example, a glioma cell divides into 2 daughter cells, or migrates through narrow extracellular spaces in the brain. In this dissertation, we assess upstream signaling to determine how ClC-3 is activated in the context of proliferation and migration. Using a combination of biophysical, biochemical, genetic, and imaging techniques, we identify several mechanisms suggesting that Ca2+/calmodulin-dependent protein kinase (CaMKII) regulates ClC-3 activity. We demonstrate that channels or ligands that increase [Ca2+]i also activate CaMKII, leading to downstream ClC-3 activation and promoting proliferation and migration. CaMKII regulation of ClC-3 is required for a critical cytoplasmic condensation checkpoint at the metaphase-anaphase transition, and inhibition of either protein leads to disrupted volume regulation and proliferation. Additionally, we found that bradykinin, a chemotactic peptide, increases glioma cell migration by activating CaMKII-dependent ClC-3 channels. Inhibition of ClC-3 or CaMKII completely blocked bradykinin-induced migration. We propose that CaMKII activation of ClC-3 is a critical mediator of cellular proliferation and migration and should be integrated into preexisting models. We speculate that [Ca2+]i may be a ""master regulator"" of both proliferation and migration by simultaneously controlling cytoskeletal proteins, kinases, and Ca2+-sensitive ion channels. Finally, our data suggest that targeting Cl- channels or bradykinin receptors on human glioma cells may be a novel therapeutic strategy for the management of malignant gliomas.

PhD

1 online resource (xi, 213 p.) :ill., digital, PDF file.

Neurobiology

Joint Health Sciences

bradykinin cell migration chloride channel ClC-3 Cl- channel

UNRESTRICTED

Advisors/Committee Members: Harald Sontheimer, Bedwell,David Kirk,Kevin Nabors,Burt Wadiche,Jacques.

Subjects/Keywords: Brain Neoplasms – metabolism<; br>; Calcium-Calmodulin-Dependent Protein Kinase Type 2 – metabolism.<; br>; Cell Movement – physiology<; br>; Chloride Channels – metabolism.<; br>; Gene Expression Regulation<; br>; Gene Expression Regulation, Enzymologic<; br>; Gene Expression Regulation, Neoplastic<; br>; Glioma – metabolism<; br>; Ion Channels – metabolism<; br>; Membrane Transport Proteins – metabolism.<; br>; Mitosis<; br>; Neoplasms – metabolism<; br>; Neoplasms – pathology

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

APA (6^th Edition):

Cuddapah, V. A. (2012). Regulation Of Clc-3 In Human Malignant Glioma. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1394

Chicago Manual of Style (16^th Edition):

Cuddapah, Vishnu Anand. “Regulation Of Clc-3 In Human Malignant Glioma.” 2012. Doctoral Dissertation, University of Alabama – Birmingham. Accessed March 07, 2021. http://contentdm.mhsl.uab.edu/u?/etd,1394.

MLA Handbook (7^th Edition):

Cuddapah, Vishnu Anand. “Regulation Of Clc-3 In Human Malignant Glioma.” 2012. Web. 07 Mar 2021.

Vancouver:

Cuddapah VA. Regulation Of Clc-3 In Human Malignant Glioma. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2012. [cited 2021 Mar 07]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1394.

Council of Science Editors:

Cuddapah VA. Regulation Of Clc-3 In Human Malignant Glioma. [Doctoral Dissertation]. University of Alabama – Birmingham; 2012. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1394

4. Kim, Min-Jung. Chloride Channels in Normal Human Blood Monocytes and a Macrophage-like Cell Line.

Degree: M.S. in Biomedical Sciences, Biomedical Sciences (graduate program), 2004, Creighton University

URL: http://hdl.handle.net/10504/47222

► Phagocytic cells serve critical roles in the body’s immune response by recognizing, phagocytosing and destroying foreign particles. A major class of phagocytic cells is composed… (more)

▼ Phagocytic cells serve critical roles in the body’s immune response by recognizing, phagocytosing and destroying foreign particles. A major class of phagocytic cells is composed of monocytes and macrophages. During inflammation there is release of several inflammatory mediators and chemokines, which attract circulating monocytes towards the endothelium. Monocytes firmly adhere to, and actively migrate through, endothelial tight junctions in order to enter tissue, where they then differentiate into macrophages and function to phagocytose apoptotic bodies and damaged cells. Migration of monocytes into tissues through endothelial tight junctions requires shape and volume change. However, the underlying mechanisms involved in monocyte shape and volume change are unclear.|Alteration in ion channels, especially chloride channels, is generally involved in the shape and volume change of circulating cells for successful invasion into tissues. In this work, we examined chloride currents in human blood monocytes and macrophages, and their role in adhesion and migration. Chloride currents were recorded in freshly isolated human blood monocytes and WBC264-9C cells (a macrophage-like cell line) using the whole-cell patch clamp technique. The effects of chloride channel blockers were then examined on chloride currents and on the migration and adhesion of human blood monocytes to vascular endothelial cells.|Whole-cell Cl' currents in human blood monocytes were outwardly rectifying and time-independent. Macrophage cell line Cl' currents were outwardly rectifying and time-dependent. Volume-sensitive chloride channel blockers, NPPB and IAA94, attenuated Cl' currents, as well as inhibited monocyte chemotaxis with similar sensitivity, as measured in a Boyden chemotactic chamber. NPPB, but not IAA94, increased cell volume (as measured by shape change) and decreased TNF-a-induced monocyte adhesion to endothelial cells. Inflammatory cytokines IL-8 and IL-12 increased Cl' currents in monocytes. IFN-y also activated Cl' currents in monocytes, but to a lesser degree than that of IL-8 and IL-12. Interestingly, IFN-y also activated Cl' currents in a macrophage-like cell line.|These results suggest that chloride channels affect monocyte migration, presumably due to changes in cell volume and shape. Inflammatory cytokines can enhance Cl' current to facilitate monocyte migration into tissues as well as to regulate macrophage function. Advisors/Committee Members: Agrawal, Devendra (advisor), Kim, Min-Jung (cuauthor).

Subjects/Keywords: Chloride Channels – physiology; Monocytes – physiology

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

APA (6^th Edition):

Kim, M. (2004). Chloride Channels in Normal Human Blood Monocytes and a Macrophage-like Cell Line. (Masters Thesis). Creighton University. Retrieved from http://hdl.handle.net/10504/47222

Chicago Manual of Style (16^th Edition):

Kim, Min-Jung. “Chloride Channels in Normal Human Blood Monocytes and a Macrophage-like Cell Line.” 2004. Masters Thesis, Creighton University. Accessed March 07, 2021. http://hdl.handle.net/10504/47222.

MLA Handbook (7^th Edition):

Kim, Min-Jung. “Chloride Channels in Normal Human Blood Monocytes and a Macrophage-like Cell Line.” 2004. Web. 07 Mar 2021.

Vancouver:

Kim M. Chloride Channels in Normal Human Blood Monocytes and a Macrophage-like Cell Line. [Internet] [Masters thesis]. Creighton University; 2004. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/10504/47222.

Council of Science Editors:

Kim M. Chloride Channels in Normal Human Blood Monocytes and a Macrophage-like Cell Line. [Masters Thesis]. Creighton University; 2004. Available from: http://hdl.handle.net/10504/47222

University of Adelaide

5. Bennetts, Brett. Structure function studies of muscle-type CIC chloride channels.

Degree: 2006, University of Adelaide

URL: http://hdl.handle.net/2440/48393

► ClC proteins are chloride channels and transporters that are found in a wide variety of prokaryotic and eukaryotic cell-types. The mammalian chloride channel ClC-1 is… (more)

▼ ClC proteins are chloride channels and transporters that are found in a wide variety of prokaryotic and eukaryotic cell-types. The mammalian chloride channel ClC-1 is an important modulator of the electrical excitability of skeletal muscle. The Torpedo electric-organ chloride channel, ClC-0 is structurally and functionally similar to ClC- 1. These proteins are referred to as the muscle-type ClC channels. The present work identifies several functional differences between the muscle type channels, and explores the structural basis of these and other previously reported differences. First the temperature dependence of ClC-1 channels was quantified. These calculations revealed distinct contrasts to previously published measurements of ClC-0 temperature sensitivity, indicating differences between the channels in the structural rearrangements associated with channel gating. Next the effect of extracellular ion substitution on ClC-0 function was examined. These measurements suggested that occupancy of an anion binding-site on the extracellular side of the selectivity-filter stabilises the open state of the channel, and that the diameter of the channel pore increases during channel opening. Three-dimensional models of the muscle-type channels were constructed based on the atomic coordinates of prokaryotic homologues. Differences in selectivity between ClC-0 and ClC-1 could be rationalised, in part, by differences in the chemistry of the narrow constriction of the channel pore. The major structural divergence between the muscle-type channels occurs in the expansive intracellular carboxy terminus. Replacing this region of ClC-1 with the corresponding region from ClC-0 resulted in distinct changes in common gating of the channel. These experiments rigorously characterise the dependence of ClC-1 function on temperature and the effect of foreign anionic-substrates on ClC-0 function. The results identify important residues involved in ionic selectivity of the channels, and validate the use of high-resolution prokaryotic channel structures as a predictive tool for studying the muscle-type channels. They also demonstrate that the carboxy-terminal of the channels is an important determinant of common gating. Advisors/Committee Members: Roberts, Michael (advisor), Rychkov, Grigori (advisor), School of Molecular and Biomedical Science : Physiology (school).

Subjects/Keywords: physiology, ion-channel, neuroscience, biophysics; Chloride channels; Ion channels

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

APA (6^th Edition):

Bennetts, B. (2006). Structure function studies of muscle-type CIC chloride channels. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/48393

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):

Bennetts, Brett. “Structure function studies of muscle-type CIC chloride channels.” 2006. Thesis, University of Adelaide. Accessed March 07, 2021. http://hdl.handle.net/2440/48393.

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

MLA Handbook (7^th Edition):

Bennetts, Brett. “Structure function studies of muscle-type CIC chloride channels.” 2006. Web. 07 Mar 2021.

Vancouver:

Bennetts B. Structure function studies of muscle-type CIC chloride channels. [Internet] [Thesis]. University of Adelaide; 2006. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2440/48393.

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

Council of Science Editors:

Bennetts B. Structure function studies of muscle-type CIC chloride channels. [Thesis]. University of Adelaide; 2006. Available from: http://hdl.handle.net/2440/48393

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

6. Amaral, Michelle Dawn. TRP-ing down a TRK : a new role for transient receptor potential channels as novel mediators of brain-derived neurotrophic factor actions at both sides of the excitatory synapse.

Degree: PhD, 2008, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,225

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Over the years, various roles for neurotrophins have been revealed, being initially described as survival signals for neurons making their initial synaptic contacts in the… (more)

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Over the years, various roles for neurotrophins have been revealed, being initially described as survival signals for neurons making their initial synaptic contacts in the developing brain. Eventually, it was discovered that these molecules also play important modulatory roles in the adult brain. The work encompassed in this dissertation serves to characterize one particular neurotrophin, brain-derived neurotrophic factor (BDNF), which has been implicated in long-term potentiation (LTP), and its effects at CA3-CA1 synapses in the hippocampus following acute application in vitro. To this end, we have demonstrated the presence of a novel, non-selective cationic current that is initiated by BDNF in hippocampal CA1 pyramidal neurons. This current, IBDNF, is activated when BDNF binds to TrkB receptors on CA1 neurons and requires activation of the PLC[gamma] and PI3K pathways for intracellular Ca2+ mobilization and vesicle exocytosis, respectively. IBDNF is mediated via cell surface membrane TRPC3 channels, assessed using TRPC channel inhibitors and siRNA specifically designed to knock-down TRPC3 mRNA levels. The quantity of cell surface TRPC3 channels was increased via exocytosis of TRPC3-containing vesicles following IBDNF activation. Simultaneous electrophysiology and Ca2+ imaging studies detected an increase in intracellular Ca2+ at proximal dendrites that preceded IBDNF activation, followed by widespread Ca2+ elevations concurrent with membrane depolarization. Activation of TrkB receptors and IP3 receptors, fullintracellular Ca2+ stores, and the presence of extracellular Ca2+ along with TRPC channels were also required for the BDNF-induced intracellular Ca2+ increase and IBDNF activation. Previously, it has been demonstrated that BDNF causes an increase in dendritic spine density in hippocampal CA1 neurons; interestingly, this effect was nullified upon siRNA knock-down of TRPC3 mRNA and also by TRPC inhibitors, suggesting an important role for TRPC3 channels in BDNF morphogenic functions. A further illustration of this is depicted by our finding that acute application of BDNF to CA3-CA1 synapses rapidly enhances presynaptic quantal transmitter release by Ca2+ mobilization from intracellular stores, a signal further amplified by Ca2+ entry through TRPC channels. Thus, the multifaceted effects of BDNF encompass both the presynapse and the postsynapse at CA3-CA1 synapses in the hippocampus.

PH.D.

xvi, 228 p. : ill., digital, PDF file.

Neurobiology

Joint Health Sciences

BDNF TRPC Hippocampus CA1 Dendritic Spines mEPSC

UNRESTRICTED

Advisors/Committee Members: Pozzo-Miller, Lucas, Benos, Dale J. , Blalock, J. Edwin , Hablitz, John J. , Theibert, Anne B..

Subjects/Keywords: Brain-Derived Neurotrophic Factor <; br>; Calcium – metabolism <; br>; Dendritic Spines – metabolism <; br>; Hippocampus <; br>; Ion Channels – physiology <; br>; Pyramidal Cells – metabolism <; br>; TRPC Cation Channels

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

APA (6^th Edition):

Amaral, M. D. (2008). TRP-ing down a TRK : a new role for transient receptor potential channels as novel mediators of brain-derived neurotrophic factor actions at both sides of the excitatory synapse. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,225

Chicago Manual of Style (16^th Edition):

Amaral, Michelle Dawn. “TRP-ing down a TRK : a new role for transient receptor potential channels as novel mediators of brain-derived neurotrophic factor actions at both sides of the excitatory synapse.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed March 07, 2021. http://contentdm.mhsl.uab.edu/u?/etd,225.

MLA Handbook (7^th Edition):

Amaral, Michelle Dawn. “TRP-ing down a TRK : a new role for transient receptor potential channels as novel mediators of brain-derived neurotrophic factor actions at both sides of the excitatory synapse.” 2008. Web. 07 Mar 2021.

Vancouver:

Amaral MD. TRP-ing down a TRK : a new role for transient receptor potential channels as novel mediators of brain-derived neurotrophic factor actions at both sides of the excitatory synapse. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2021 Mar 07]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,225.

Council of Science Editors:

Amaral MD. TRP-ing down a TRK : a new role for transient receptor potential channels as novel mediators of brain-derived neurotrophic factor actions at both sides of the excitatory synapse. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,225

7. Albertson, Asher J. HCN channels and regulation of neocortical network activity.

Degree: PhD, 2012, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,1133

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Hyperpolarization activated non-specifc cation (HCN) channels are unique channels that activate following membrane hyperpolarization. Expressed primarily along the apical dendrites of pyramidal neurons, they pass… (more)

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Hyperpolarization activated non-specifc cation (HCN) channels are unique channels that activate following membrane hyperpolarization. Expressed primarily along the apical dendrites of pyramidal neurons, they pass a non-inactivating, inward current (Ih). HCN channel activation at resting membrane potentials profoundly impacts the synaptic and intrinsic properties of pyramidal neurons. Activated channels decrease intrinsic membrane excitability, hyperpolarize the resting membrane potential, and increase excitatory post-synaptic potentials (EPSP) summation. Loss of HCN channels is commonly observed in models of epilepsy. This dissertation tests the hypothesis that the influence of HCN channels on individual neuron excitability translates to an influence on network excitability. Furthermore, we hypothesize that loss of HCN channels in a model of malformation epilepsy contributes to observed hyperexcitability. We found that rats with freeze induced cortical lesions, a well-established model of malformation epilepsy, have reduced Ih, significantly increased EPSP summation, and increased membrane excitability. Using voltage sensitive dye imaging, we found that freeze lesioned rats exhibit significantly increased network excitability. Inhibiting HCN channels with ZD 7288 similarly increases network activation. Enhancing HCN channels with the anticonvulsant lamotrigine reduces network excitability. The ability of lamotrigine to reduce network excitability is significantly reduced in freeze lesioned rats. We next examined whether HCN channels influence epileptiform network events. Epileptiform events were evoked in situ using strong stimulation in disinhibited acute cortical slices. We found that HCN channel inhibition significantly increases the area of epileptiform events in pyramidal neurons from layers 5 and 2/3 and well as interneurons from layers 5 and 1. Interesting, ZD 7288 also increases the number of action potentials overlying epileptiform events, but only in layer five pyramidal neurons. This increase in area is mimicked when neurons are voltage clamped at -60 mV indicating that the increase in area is a network effect. We also found reduced Ih in layer 5 interneurons in freeze lesioned rats. ZD 7288 increases summation in layer 5 interneurons from control, but not lesioned rats. HCN channel inhibition decreases interneuron membrane excitability, and rats with freeze lesions have reduced baseline membrane excitability.

1 online resource (ix, 156 p.) : ill., digital, PDF file.

Neurobiology;

Joint Health Sciences;

HCN Channels Ih ZD 7288 Lamotrigine Epilepsy Cortical Dysplasia

UNRESTRICTED

Advisors/Committee Members: Hablitz, John J., Engler, Jeff , Wadiche, Linda , McMahon, Lori , Pozzo-Miller, Lucas.

Subjects/Keywords: Cerebral Cortex – physiopathology<; br>; Cyclic Nucleotide-Gated Cation Channels – physiology<; br>; Epilepsy – drug therapy<; br>; Epilepsy – physiopathology<; br>; Excitatory Postsynaptic Potentials<; br>; Malformations of Cortical Development – physiopathology<; br>; Pyramidal Cells – physiology

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

APA (6^th Edition):

Albertson, A. J. (2012). HCN channels and regulation of neocortical network activity. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1133

Chicago Manual of Style (16^th Edition):

Albertson, Asher J. “HCN channels and regulation of neocortical network activity.” 2012. Doctoral Dissertation, University of Alabama – Birmingham. Accessed March 07, 2021. http://contentdm.mhsl.uab.edu/u?/etd,1133.

MLA Handbook (7^th Edition):

Albertson, Asher J. “HCN channels and regulation of neocortical network activity.” 2012. Web. 07 Mar 2021.

Vancouver:

Albertson AJ. HCN channels and regulation of neocortical network activity. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2012. [cited 2021 Mar 07]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1133.

Council of Science Editors:

Albertson AJ. HCN channels and regulation of neocortical network activity. [Doctoral Dissertation]. University of Alabama – Birmingham; 2012. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1133

8. Sarfare, Shanta. Overexpression of GARP2 increases phototransduction gain.

Degree: PhD, 2010, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,922

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The cGMP-gated cation channel (CNG) in the rod photoreceptors is an essential component of phototransduction, and may have a role in maintaining structural integrity of… (more)

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The cGMP-gated cation channel (CNG) in the rod photoreceptors is an essential component of phototransduction, and may have a role in maintaining structural integrity of the rod outer segment (ROS). The β-subunit of the CNG channel (CNGB1) in the rod photoreceptors is comprised of an N-terminal glutamic acid-rich region (GARP’) and a Cterminal channel-like region. Additionally, two soluble proteins GARP1 and GARP2 are alternatively spliced from the CNGB1 gene. Although GARPs are known to interact with other proteins in the rod photoreceptors, their role is currently unknown. To determine the role of GARP2 in the rod photoreceptors, we generated transgenic mice expressing GARP2 (GARP2 tg). Our results show that GARP2 alone could not rescue the structural phenotype of the CNGB1 knockout, suggesting that more than one GARP-region containing protein or the β-subunit of the CNG channel is necessary, and that GARP2 by itself is not sufficient to promote proper ROS structural integrity. GARP2 was expressed three-fold over the wild type in the GARP2 tg and it was correctly localized to the rim region of the ROS. Other ROS proteins examined were also properly localized and their expression levels were unchanged, except for the channel α-subunit, which was slightly elevated. Abnormally elongated membranes were occasionally observed in the outer segments of the GARP2 tg, which were also shorter than wild type rods. ERG analysis revealed that at 1 month, the average maximum rod a-wave responses were decreased 33%, which may be attributed to a reduced ROS length. The half-maximum rod sensitivity was unchanged in the GARP2 tg mice, indicating normal rod function. The parameter S derived from a fit to the rod phototransduction model was increased more than 50%, indicating an increase in phototransduction gain. Our findings suggest that GARP2 has a dual function in ROS: a structural role in proper rod outer segment disk morphogenesis and maintenance of structural integrity, and a functional role in regulating the activation phase of phototransduction.

1 online resource (x, 113 p. : ill., digital, PDF file)

Vision Science;

Optometry;

Retina Transgenic mice Disk morphogenesis Phototransduction Photoreceptor Cyclic-nucleotide gated channel

UNRESTRICTED

Advisors/Committee Members: Keyser, Kent T., Pittler, Steven J. , Kraft, Timothy W. , Bross, Alecia K. , Wang, Shu-Zhen.

Subjects/Keywords: Cyclic GMP – physiology<; br>; Cyclic Nucleotide-Gated Cation Channels<; br>; Light Signal Transduction<; br>; Mice, Transgenic<; br>; Photoreceptor Cells<; br>; Retina<; br>; Retinal Rod Photoreceptor Cells – physiology

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

APA (6^th Edition):

Sarfare, S. (2010). Overexpression of GARP2 increases phototransduction gain. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,922

Chicago Manual of Style (16^th Edition):

Sarfare, Shanta. “Overexpression of GARP2 increases phototransduction gain.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed March 07, 2021. http://contentdm.mhsl.uab.edu/u?/etd,922.

MLA Handbook (7^th Edition):

Sarfare, Shanta. “Overexpression of GARP2 increases phototransduction gain.” 2010. Web. 07 Mar 2021.

Vancouver:

Sarfare S. Overexpression of GARP2 increases phototransduction gain. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2021 Mar 07]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,922.

Council of Science Editors:

Sarfare S. Overexpression of GARP2 increases phototransduction gain. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,922

9. Gaurav, Rohit. Chloride Channel 3 (CLC3), an Immune Antiporter in the Migration and Activation of Human Eosinophils in Allergic Asthma.

Degree: PhD, Biomedical Sciences (graduate program), 2014, Creighton University

URL: http://hdl.handle.net/10504/62868

► Allergic asthma is a complex and heterogeneous disease of the airways. Eosinophils migrate to the airways under the influence of chemokines to start an excessive… (more)

▼ Allergic asthma is a complex and heterogeneous disease of the airways. Eosinophils migrate to the airways under the influence of chemokines to start an excessive damage and repair cycle leading to airway inflammation and remodeling in allergic asthma. TGF-β has been closely related with eosinophils in airway remodeling. Eosinophils produce TGF-β; at the same time they are also affected by TGF-β, leading to their migration and activation. TGF-β has also been implicated in the modulation of chloride channels including CLC3, which is required for the respiratory burst by eosinophils and neutrophils, and altering the shape to cause migration of neutrophils. However, the underlying mechanism of eosinophil migration and activation is not clearly understood.|In this study, the expression and roles of CLC3 in human eosinophils were investigated. Novel transcript variants of CLC3 in human peripheral blood eosinophils were found and compared among healthy, mild-to-moderate, and moderate-to-severe asthmatics. Higher expression of CLC3 was noted in blood eosinophils of mild-to-moderate asthmatics compared to the healthy counterparts. The expression was even higher than the moderate-to-severe asthmatic group. On the contrary, nasal lavage eosinophils showed higher CLC3 expression in moderate-to-severe asthmatics than mild-to-moderate. The CLC3 expression was noted in the membrane and organelles of eosinophils suggesting a broad role of this chloride channel in the pathophysiology of allergic asthma. Using different blockers and techniques, TGF-β and eotaxin-induced migration and activation of eosinophils were found to be dependent on CLC3.|Molecular investigation revealed that TGF-β regulates CLC3 through PKC-δ and SMAD3. Gene analysis disclosed multiple AP-1 binding sites on CLC3 gene, suggesting an important role of AP-1 in the regulation of CLC3. Using different bioinformatics tools, an uncharacterized CLC3 promoter was identified and cloned. Promoter activity assay confirmed AP-1 as a major regulator CLC3.|Identification of novel transcript variants of CLC3 and their role in allergic asthma in addition to the signaling events regulating CLC3 will help in understanding the underlying signaling events taking place in the activation and migration of eosinophils through CLC3. CLC3 transcript variants may serve as biomarkers for the identification of asthma phenotypes. Moreover, studying the complex interactions of these proteins in hyper-activated eosinophils may help in understanding the pathophysiology of allergic asthma and provide a potential therapeutic approach in allergic asthma. Advisors/Committee Members: Agrawal, Devendra K. (advisor), Gaurav, Rohit (cuauthor).

Subjects/Keywords: Chloride Channels – metabolism; Asthma – immunology; Airway Inflammation

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APA (6^th Edition):

Gaurav, R. (2014). Chloride Channel 3 (CLC3), an Immune Antiporter in the Migration and Activation of Human Eosinophils in Allergic Asthma. (Doctoral Dissertation). Creighton University. Retrieved from http://hdl.handle.net/10504/62868

Chicago Manual of Style (16^th Edition):

Gaurav, Rohit. “Chloride Channel 3 (CLC3), an Immune Antiporter in the Migration and Activation of Human Eosinophils in Allergic Asthma.” 2014. Doctoral Dissertation, Creighton University. Accessed March 07, 2021. http://hdl.handle.net/10504/62868.

MLA Handbook (7^th Edition):

Gaurav, Rohit. “Chloride Channel 3 (CLC3), an Immune Antiporter in the Migration and Activation of Human Eosinophils in Allergic Asthma.” 2014. Web. 07 Mar 2021.

Vancouver:

Gaurav R. Chloride Channel 3 (CLC3), an Immune Antiporter in the Migration and Activation of Human Eosinophils in Allergic Asthma. [Internet] [Doctoral dissertation]. Creighton University; 2014. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/10504/62868.

Council of Science Editors:

Gaurav R. Chloride Channel 3 (CLC3), an Immune Antiporter in the Migration and Activation of Human Eosinophils in Allergic Asthma. [Doctoral Dissertation]. Creighton University; 2014. Available from: http://hdl.handle.net/10504/62868

Columbia University

10. Mao, De Yu. Chloride Intracellular Channel (CLIC) proteins function to modulate Rac1 and RhoA downstream of endothelial G-protein coupled receptors signaling.

Degree: 2019, Columbia University

URL: https://doi.org/10.7916/d8-eyrq-5w43

► Chloride intracellular channel proteins have homology to ion channels and omega class of glutathione-S-transferases but channel activity is not well established, suggesting roles in other… (more)

▼ Chloride intracellular channel proteins have homology to ion channels and omega class of glutathione-S-transferases but channel activity is not well established, suggesting roles in other signaling pathways. Among the six CLICs, CLIC1 and CLIC4 are expressed in endothelial cells (EC) and act to promote EC proliferation, capillary-like networks, and lumen formation. We and others determined that Sphingosine-1-phosphate (S1P) signaling promotes transient CLIC4 membrane localization. We report that CLIC1 and CLIC4 have distinct roles in endothelial S1P signaling. In knockdown studies, CLIC1 and CLIC4 were independently required for S1PR1-mediated Rac1 activation, enhanced EC barrier integrity, and EC migration. CLIC1 was uniquely required for S1PR2/3-driven RhoA activation and actin stress fiber formation, while CLIC4 was uniquely required for thrombin/PAR-driven RhoA activation and endothelial permeability. CLICs were not required for other GPCR-mediated pathways measured, including S1PR1-mediated cAMP regulation downstream of Gαi, or Ras and ERK activation downstream of Gβγ. Endothelial β-adrenergic signaling, which uses Gαs, was unaltered by loss of CLICs. Further investigation of receptor tyrosine kinase signaling (VEGF, EGF) in endothelial cells reveals their signaling cascades do not depend on CLICs as well. We conclude that CLICs mediate S1PR-driven RhoA and Rac1 regulation, and thrombin/PAR-driven RhoA activation, and a possible mediator for endothelial GPCR by modulating Rac1 and RhoA. CLIC N-termini contain membrane insertion motifs and the putative ion channel domain, while the C-termini contain two predicted SH domains. Chimeric proteins generated by swapping N and C-termini of CLIC1 and CLIC4 were used in rescue experiments. The C-terminal domain was determined to confer S1PR1-CLIC-Rac1 mediated barrier function and migration. We further characterized N-termini of CLIC4 and membrane localization of by generating CLIC4 C-termini truncated protein, along with CLIC4 C-termini fusing with Lck-peptide for myristylation and plasma membrane re-localization. CLIC4 C-termini alone fails to rescue S1PR1-CLIC-Rac1 mediated barrier function, while membrane localization of the CLIC4 C-terminal domain functions in S1P signaling, suggesting the N-terminal domain confers membrane localization but not signaling function. Thus, we conclude S1P promotes cell localization of CLIC4 to the EC plasma membrane through N-termini, which then regulates Rac1 mediated events through C-termini. Through these findings, our work defines a molecular mechanism through which CLICs function in endothelium.

Subjects/Keywords: Pharmacology; Chloride channels; Molecular biology; Cytology

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

APA (6^th Edition):

Mao, D. Y. (2019). Chloride Intracellular Channel (CLIC) proteins function to modulate Rac1 and RhoA downstream of endothelial G-protein coupled receptors signaling. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/d8-eyrq-5w43

Chicago Manual of Style (16^th Edition):

Mao, De Yu. “Chloride Intracellular Channel (CLIC) proteins function to modulate Rac1 and RhoA downstream of endothelial G-protein coupled receptors signaling.” 2019. Doctoral Dissertation, Columbia University. Accessed March 07, 2021. https://doi.org/10.7916/d8-eyrq-5w43.

MLA Handbook (7^th Edition):

Mao, De Yu. “Chloride Intracellular Channel (CLIC) proteins function to modulate Rac1 and RhoA downstream of endothelial G-protein coupled receptors signaling.” 2019. Web. 07 Mar 2021.

Vancouver:

Mao DY. Chloride Intracellular Channel (CLIC) proteins function to modulate Rac1 and RhoA downstream of endothelial G-protein coupled receptors signaling. [Internet] [Doctoral dissertation]. Columbia University; 2019. [cited 2021 Mar 07]. Available from: https://doi.org/10.7916/d8-eyrq-5w43.

Council of Science Editors:

Mao DY. Chloride Intracellular Channel (CLIC) proteins function to modulate Rac1 and RhoA downstream of endothelial G-protein coupled receptors signaling. [Doctoral Dissertation]. Columbia University; 2019. Available from: https://doi.org/10.7916/d8-eyrq-5w43

11. Wadiche, Jacques Isaac. Properties of cloned excitatory amino acid transporters.

Degree: PhD, 1998, Oregon Health Sciences University

URL: doi:10.6083/M43N21MJ ; http://digitalcommons.ohsu.edu/etd/2592

Subjects/Keywords: Excitatory Amino Acids; Cloning, Molecular; Carrier Proteins; Chloride Channels – physiology

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

APA (6^th Edition):

Wadiche, J. I. (1998). Properties of cloned excitatory amino acid transporters. (Doctoral Dissertation). Oregon Health Sciences University. Retrieved from doi:10.6083/M43N21MJ ; http://digitalcommons.ohsu.edu/etd/2592

Chicago Manual of Style (16^th Edition):

Wadiche, Jacques Isaac. “Properties of cloned excitatory amino acid transporters.” 1998. Doctoral Dissertation, Oregon Health Sciences University. Accessed March 07, 2021. doi:10.6083/M43N21MJ ; http://digitalcommons.ohsu.edu/etd/2592.

MLA Handbook (7^th Edition):

Wadiche, Jacques Isaac. “Properties of cloned excitatory amino acid transporters.” 1998. Web. 07 Mar 2021.

Vancouver:

Wadiche JI. Properties of cloned excitatory amino acid transporters. [Internet] [Doctoral dissertation]. Oregon Health Sciences University; 1998. [cited 2021 Mar 07]. Available from: doi:10.6083/M43N21MJ ; http://digitalcommons.ohsu.edu/etd/2592.

Council of Science Editors:

Wadiche JI. Properties of cloned excitatory amino acid transporters. [Doctoral Dissertation]. Oregon Health Sciences University; 1998. Available from: doi:10.6083/M43N21MJ ; http://digitalcommons.ohsu.edu/etd/2592

University of Hong Kong

12. Lu, Lin. The involvement of connexin hemichannels and cystic fibrosis transmembrane conductance regulator in acidosis-induced ATP release from skeletal myocytes.

Degree: 2014, University of Hong Kong

URL: http://hdl.handle.net/10722/208017

► The cystic fibrosis transmembrane conductance regulator (CFTR) was identified to be involved in acidosis-induced ATP release from skeletal myocytes in vitro and from contracting muscle… (more)

▼ The cystic fibrosis transmembrane conductance regulator (CFTR) was identified to be involved in acidosis-induced ATP release from skeletal myocytes in vitro and from contracting muscle in vivo. My PhD studies aimed to investigate the underlying mechanism and identify the pathway for ATP release in acidosis-induced CFTR-regulated ATP release. Lactic acid (10 mM) decreased the intracellular pH of L6 skeletal myocytes to 6.87 ± 0.12 after 3 hours, and the lowered pH resulted in the elevation of ATP release from skeletal myocytes. The acidosis-induced ATP release was totally abolished by GlyH-101 (40 μM), an open-channel CFTR blocker, suggesting that CFTR was involved. The cAMP/PKA signaling pathway was involved in the CFTR-regulated ATP release from skeletal myocytes: 1). Forskolin increased the extracellular ATP and the phosphorylation of CFTR; IBMX, a phosphodiesterase inhibitor, further enhanced the forskolin-induced extracellular ATP and phosphorylation of CFTR; 2). Inhibition of PKA by its selective inhibitor KT-5720 abolished the acidosis-induced ATP release and the forskolin-induced phosphorylation of CFTR. In addition, the inhibition of Na+/H+ exchanger (NHE) by amiloride, or inhibition of Na+/Ca2+ exchanger (NCX) by its specific inhibitors SN-6 and KB-R7943 abolished the lactic-acid-induced ATP release from skeletal myocytes, indicating that NHE and NCX might be involved. Previous studies demonstrated that Connexin hemichannels and Pannexin channels were able to conduct ATP in response to stimuli. This study found that connexin 43 (Cx43) was strongly expressed on skeletal myocytes, while Pannexin 1 (Panx1) showed a strong expression in gastrocnemius muscle. Investigation of the role that Cx43 may play in acidosis-induced cAMP/PKA-activated CFTR-regulated ATP release from myocytes showed that: 1). Cx43 was immunoprecipitated with CFTR suggesting a physical interaction; 2). The opening of Cx hemichannels was increased by lactic acid and this lactic-acid-induced opening was inhibited by CFTRinh-172, suggesting the mediation of CFTR; 3). Inhibition of Cxs and Panxs with carbenoxolone abolished the acidosis-induced ATP release; moreover, specific silencing of the Cx43 gene using siRNA decreased both basal and acidosis-induced ATP release, suggesting that Cx43 was involved; 4). Overexpression of CFTR alone did not elevate the acidosis-induced ATP release, while overexpression of Cx43 alone doubled the acidosis-induced ATP, and co-overexpression of CFTR and Cx43 further elevated the acidosis-induced ATP release, supporting the concept that Cx43 functionally interacted with CFTR to induce the acidosis-induced ATP release. Panx1 was studied in native skeletal muscle, and found to be coimmunoprecipitated with CFTR. Inhibition of Panxs with gadolinium or probenecid abolished the muscle-contraction-induced ATP release, while inhibition with carbenoxolone or quinine reduced it to less than 10% of control, suggesting that Panx1 may be involved in the acidosis-induced ATP release during muscle contraction. All the… Advisors/Committee Members: Ballard, HJ (advisor), Li, GR (advisor).

Subjects/Keywords: Muscle cells - Physiology; Cystic fibrosis - Pathophysiology; Connexins; Chloride channels; Adenosine triphosphate

Record Details Similar Records Cite « Share

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

APA (6^th Edition):

Lu, L. (2014). The involvement of connexin hemichannels and cystic fibrosis transmembrane conductance regulator in acidosis-induced ATP release from skeletal myocytes. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/208017

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):

Lu, Lin. “The involvement of connexin hemichannels and cystic fibrosis transmembrane conductance regulator in acidosis-induced ATP release from skeletal myocytes.” 2014. Thesis, University of Hong Kong. Accessed March 07, 2021. http://hdl.handle.net/10722/208017.

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

MLA Handbook (7^th Edition):

Lu, Lin. “The involvement of connexin hemichannels and cystic fibrosis transmembrane conductance regulator in acidosis-induced ATP release from skeletal myocytes.” 2014. Web. 07 Mar 2021.

Vancouver:

Lu L. The involvement of connexin hemichannels and cystic fibrosis transmembrane conductance regulator in acidosis-induced ATP release from skeletal myocytes. [Internet] [Thesis]. University of Hong Kong; 2014. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/10722/208017.

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

Council of Science Editors:

Lu L. The involvement of connexin hemichannels and cystic fibrosis transmembrane conductance regulator in acidosis-induced ATP release from skeletal myocytes. [Thesis]. University of Hong Kong; 2014. Available from: http://hdl.handle.net/10722/208017

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

University of Hong Kong

13. Cai, Weisong. Cystic fibrosis transmembrane conductance regulator is involved in therelease of ATP from contracting skeletal muscle.

Degree: 2012, University of Hong Kong

URL: http://hdl.handle.net/10722/180987

► Contracting skeletal muscle releases ATP into the interstitial space where it is subsequently broken down to adenosine by the action of ecto-5’-nucleotidase. Both ATP and… (more)

▼ Contracting skeletal muscle releases ATP into the interstitial space where it is subsequently broken down to adenosine by the action of ecto-5’-nucleotidase. Both ATP and adenosine are vasodilators that contribute to the exercise hyperaemia. However, the mechanism for the release of ATP from muscle during exercise remains unknown. Cystic fibrosis transmembrane conductance regulator (CFTR) is involved in ATP release from muscle at low intracellular pH: this study was performed to investigate whether CFTR was involved in the ATP release from skeletal muscle during contractions. Experiments were performed in rats anaesthetised with sodium pentobarbitone and breathing spontaneously. A microdialysis probe was placed in one gastrocnemius muscle: ATP was determined in interstitial microdialysate samples using a bioluminescence assay. The sciatic nerve was stimulated to induce two bouts of muscle contractions, separated by a recovery period of 40 mins; one of the inhibitors was administered prior to the second bout of contractions. Muscle contractions elevated the interstitial ATP by 1500 to 3000%. In the control experiments, no drug was given: both the contractile force and the increase in interstitial ATP were reproducible in repeated contraction bouts. Infusion of a specific inhibitor of CFTR, CFTRinh-172, did not alter the contractile force, but significantly lowered the interstitial ATP during muscle contractions, suggesting that CFTR was involved in the contraction-induced ATP release. Similarly, infusion of the Protein Kinase A inhibitor, KT5720, significantly reduced interstitial ATP during muscle contractions without altering contractile force, suggesting that CFTR in skeletal muscle is activated through the cAMP/PKA pathway. The increase in interstitial ATP during muscle contraction was also inhibited by the Na/H exchanger inhibitor, amiloride, or the Na/Ca exchanger inhibitor, SN6. It has been also shown that two gap junction hemichannel inhibitors, gadolinium and carbenoxolone, could attenuate the increase of ATP during muscle contraction. These data suggest that CFTR, activated through the cAMP/protein kinase A pathway, is involved in the ATP release during muscle contraction, and that activation of the Na/H exchanger and Na/Ca exchanger was also required, indicating that the signal transduction mechanism for CFTR activation during muscle contractions may be similar to that which is reported to occur at low pH. The preliminary data showed that the gap junction hemichannels might mediate the ATP release from skeletal muscle cells during muscle contraction. Advisors/Committee Members: Ballard, HJ (advisor).

Subjects/Keywords: Cystic fibrosis - Pathophysiology.; Muscle contraction - Physiology.; Adenosine triphosphate.; Chloride channels.

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

APA (6^th Edition):

Cai, W. (2012). Cystic fibrosis transmembrane conductance regulator is involved in therelease of ATP from contracting skeletal muscle. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/180987

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):

Cai, Weisong. “Cystic fibrosis transmembrane conductance regulator is involved in therelease of ATP from contracting skeletal muscle.” 2012. Thesis, University of Hong Kong. Accessed March 07, 2021. http://hdl.handle.net/10722/180987.

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

MLA Handbook (7^th Edition):

Cai, Weisong. “Cystic fibrosis transmembrane conductance regulator is involved in therelease of ATP from contracting skeletal muscle.” 2012. Web. 07 Mar 2021.

Vancouver:

Cai W. Cystic fibrosis transmembrane conductance regulator is involved in therelease of ATP from contracting skeletal muscle. [Internet] [Thesis]. University of Hong Kong; 2012. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/10722/180987.

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

Council of Science Editors:

Cai W. Cystic fibrosis transmembrane conductance regulator is involved in therelease of ATP from contracting skeletal muscle. [Thesis]. University of Hong Kong; 2012. Available from: http://hdl.handle.net/10722/180987

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

University of Hong Kong

14. 冼世隆. Chloride channel in glioma cell invasion.

Degree: 2008, University of Hong Kong

URL: http://hdl.handle.net/10722/54467

Subjects/Keywords: Gliomas.; Chloride channels.; Cancer invasiveness.

Record Details Similar Records Cite « Share

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

APA (6^th Edition):

冼世隆.. (2008). Chloride channel in glioma cell invasion. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/54467

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

Chicago Manual of Style (16^th Edition):

冼世隆.. “Chloride channel in glioma cell invasion.” 2008. Thesis, University of Hong Kong. Accessed March 07, 2021. http://hdl.handle.net/10722/54467.

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

MLA Handbook (7^th Edition):

冼世隆.. “Chloride channel in glioma cell invasion.” 2008. Web. 07 Mar 2021.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

冼世隆.. Chloride channel in glioma cell invasion. [Internet] [Thesis]. University of Hong Kong; 2008. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/10722/54467.

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

Council of Science Editors:

冼世隆.. Chloride channel in glioma cell invasion. [Thesis]. University of Hong Kong; 2008. Available from: http://hdl.handle.net/10722/54467

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

University of California – San Francisco

15. Wang, Lynn. Functional Studies of the TMEM16B Calcium-activated Chloride Channel in the Lateral Septum.

Degree: Neuroscience, 2018, University of California – San Francisco

URL: http://www.escholarship.org/uc/item/9tp5r4tm

► The lateral septum (LS) plays an important role in regulating aggression. It is well recognized that LS lesions lead to a dramatic increase in aggressive… (more)

Subjects/Keywords: Neurosciences; ano2; anoctamin2; calcium-activated chloride channels; lateral septum; tmem16b

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

APA (6^th Edition):

Wang, L. (2018). Functional Studies of the TMEM16B Calcium-activated Chloride Channel in the Lateral Septum. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/9tp5r4tm

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):

Wang, Lynn. “Functional Studies of the TMEM16B Calcium-activated Chloride Channel in the Lateral Septum.” 2018. Thesis, University of California – San Francisco. Accessed March 07, 2021. http://www.escholarship.org/uc/item/9tp5r4tm.

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

MLA Handbook (7^th Edition):

Wang, Lynn. “Functional Studies of the TMEM16B Calcium-activated Chloride Channel in the Lateral Septum.” 2018. Web. 07 Mar 2021.

Vancouver:

Wang L. Functional Studies of the TMEM16B Calcium-activated Chloride Channel in the Lateral Septum. [Internet] [Thesis]. University of California – San Francisco; 2018. [cited 2021 Mar 07]. Available from: http://www.escholarship.org/uc/item/9tp5r4tm.

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

Council of Science Editors:

Wang L. Functional Studies of the TMEM16B Calcium-activated Chloride Channel in the Lateral Septum. [Thesis]. University of California – San Francisco; 2018. Available from: http://www.escholarship.org/uc/item/9tp5r4tm

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

University of Toronto

16. Harvey, Kordan. The Role of Chloride Channels in Remote Ischemic Preconditioning of Ventricular Cardiomyocytes.

Degree: 2012, University of Toronto

URL: http://hdl.handle.net/1807/33748

►

Sarcolemmal chloride channels and associated cell volume regulatory pathways have been shown to be important in local ischemic preconditioning (IPC) induced protection against myocardial ischemia/reperfusion… (more)

Subjects/Keywords: remote preconditioning; cardiomyocytes; chloride channels; volume regulation; IAA-94; 0379

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

APA (6^th Edition):

Harvey, K. (2012). The Role of Chloride Channels in Remote Ischemic Preconditioning of Ventricular Cardiomyocytes. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/33748

Chicago Manual of Style (16^th Edition):

Harvey, Kordan. “The Role of Chloride Channels in Remote Ischemic Preconditioning of Ventricular Cardiomyocytes.” 2012. Masters Thesis, University of Toronto. Accessed March 07, 2021. http://hdl.handle.net/1807/33748.

MLA Handbook (7^th Edition):

Harvey, Kordan. “The Role of Chloride Channels in Remote Ischemic Preconditioning of Ventricular Cardiomyocytes.” 2012. Web. 07 Mar 2021.

Vancouver:

Harvey K. The Role of Chloride Channels in Remote Ischemic Preconditioning of Ventricular Cardiomyocytes. [Internet] [Masters thesis]. University of Toronto; 2012. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/1807/33748.

Council of Science Editors:

Harvey K. The Role of Chloride Channels in Remote Ischemic Preconditioning of Ventricular Cardiomyocytes. [Masters Thesis]. University of Toronto; 2012. Available from: http://hdl.handle.net/1807/33748

17. M. Setti. SHEDDING LIGHT ON GLIOBLASTOMA AND DERIVED EXTRACELLULAR VESICLES IN ONE CLIC.

Degree: 2015, Università degli Studi di Milano

URL: http://hdl.handle.net/2434/264914

► ABSTRACT The treatment of glioblastoma (GBM) still represents a tremendous clinical challenge, with the average survival that is not exceeding 14 months. Given the lack… (more)

▼ ABSTRACT The treatment of glioblastoma (GBM) still represents a tremendous clinical challenge, with the average survival that is not exceeding 14 months. Given the lack of reliable prognostic markers and druggable targets in GBM, several years ago our lab’s interest focused on Chloride intracellular channel-1 (CLIC1), a protein belonging to a class of chloride channels that does not fit the classical paradigm of ion channels proteins. CLIC1 proteins can exist as both soluble globular protein and integral membrane protein with ion channel function. Upon oxidative stress, CLIC1 translocates from the cytoplasm to the plasma membrane where it exerts its function as a chloride (Cl-) channel. CLIC1 is overexpressed in several human solid tumors, including gliomas. In this study we demonstrated that CLIC1 silencing in cancer stem cells (CSCs) isolated from human GBM patients negatively influences both proliferative capacity and self-renewal properties in vitro and impairs the in vivo tumorigenic potential. Moreover, CLIC1 expression inversely associates with GBM patient survival, thus suggesting a potential exploitation of CLIC1 as a new molecular therapeutic target and a possible outcome predictor. CLIC1 has been identified as a secreted protein and detected in exosomes released from different cell types, including primary tumors. Extracellular vesicles (40-1000 nm) (EVs) are secreted by virtually all cell types that arise from the invagination and the budding of the limiting membrane of late endosomes (hence called multivesicular bodies, MVB). We showed that CLIC1 is a protein localized within EVs isolated by GBM cell lines and GBM-derived CSCs and by tuning CLIC1 expression within EVs it is possible to modulate cellular response to EVs both in vitro and in vivo. Taken together, our data suggest that CLIC1 plays an important role in regulating GBM proliferation and tumorigenic status, experimental evidences hint the possible transmission of these features to recipient cells by EV secretion. Advisors/Committee Members: supervisor: G. Pelicci, cosupervisor: R. Bjerkvig.

Subjects/Keywords: glioblastoma; chloride channels; extracellular vesicles; Settore BIO/11 - Biologia Molecolare

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

APA (6^th Edition):

Setti, M. (2015). SHEDDING LIGHT ON GLIOBLASTOMA AND DERIVED EXTRACELLULAR VESICLES IN ONE CLIC. (Thesis). Università degli Studi di Milano. Retrieved from http://hdl.handle.net/2434/264914

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):

Setti, M.. “SHEDDING LIGHT ON GLIOBLASTOMA AND DERIVED EXTRACELLULAR VESICLES IN ONE CLIC.” 2015. Thesis, Università degli Studi di Milano. Accessed March 07, 2021. http://hdl.handle.net/2434/264914.

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

MLA Handbook (7^th Edition):

Setti, M.. “SHEDDING LIGHT ON GLIOBLASTOMA AND DERIVED EXTRACELLULAR VESICLES IN ONE CLIC.” 2015. Web. 07 Mar 2021.

Vancouver:

Setti M. SHEDDING LIGHT ON GLIOBLASTOMA AND DERIVED EXTRACELLULAR VESICLES IN ONE CLIC. [Internet] [Thesis]. Università degli Studi di Milano; 2015. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2434/264914.

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

Council of Science Editors:

Setti M. SHEDDING LIGHT ON GLIOBLASTOMA AND DERIVED EXTRACELLULAR VESICLES IN ONE CLIC. [Thesis]. Università degli Studi di Milano; 2015. Available from: http://hdl.handle.net/2434/264914

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

University of California – San Francisco

18. Wong, Xiu Ming. CG16718, A Calcium-Activated Chloride Channel of the TMEM16 Family in Drosophila melanogaster.

Degree: Chemistry and Chemical Biology, 2013, University of California – San Francisco

URL: http://www.escholarship.org/uc/item/4jd0m5gb

► TMEM16A and TMEM16B are calcium-activated chloride channels (CaCCs) with important functions in mammalian physiology. Whether distant relatives of the vertebrate TMEM16 families also form CaCCs… (more)

Subjects/Keywords: Biology; Calcium-activated chloride channels; Drosophila; host defense

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APA (6^th Edition):

Wong, X. M. (2013). CG16718, A Calcium-Activated Chloride Channel of the TMEM16 Family in Drosophila melanogaster. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/4jd0m5gb

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):

Wong, Xiu Ming. “CG16718, A Calcium-Activated Chloride Channel of the TMEM16 Family in Drosophila melanogaster.” 2013. Thesis, University of California – San Francisco. Accessed March 07, 2021. http://www.escholarship.org/uc/item/4jd0m5gb.

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

MLA Handbook (7^th Edition):

Wong, Xiu Ming. “CG16718, A Calcium-Activated Chloride Channel of the TMEM16 Family in Drosophila melanogaster.” 2013. Web. 07 Mar 2021.

Vancouver:

Wong XM. CG16718, A Calcium-Activated Chloride Channel of the TMEM16 Family in Drosophila melanogaster. [Internet] [Thesis]. University of California – San Francisco; 2013. [cited 2021 Mar 07]. Available from: http://www.escholarship.org/uc/item/4jd0m5gb.

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

Council of Science Editors:

Wong XM. CG16718, A Calcium-Activated Chloride Channel of the TMEM16 Family in Drosophila melanogaster. [Thesis]. University of California – San Francisco; 2013. Available from: http://www.escholarship.org/uc/item/4jd0m5gb

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

University of Adelaide

19. Astill, David St. John. Characteristics of baculovirus - expressed in CIC-1 / by David St.John Astill.

Degree: 1996, University of Adelaide

URL: http://hdl.handle.net/2440/18707

Subjects/Keywords: 571.64/1 21; Chloride channels.

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APA (6^th Edition):

Astill, D. S. J. (1996). Characteristics of baculovirus - expressed in CIC-1 / by David St.John Astill. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/18707

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):

Astill, David St John. “Characteristics of baculovirus - expressed in CIC-1 / by David St.John Astill.” 1996. Thesis, University of Adelaide. Accessed March 07, 2021. http://hdl.handle.net/2440/18707.

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

MLA Handbook (7^th Edition):

Astill, David St John. “Characteristics of baculovirus - expressed in CIC-1 / by David St.John Astill.” 1996. Web. 07 Mar 2021.

Vancouver:

Astill DSJ. Characteristics of baculovirus - expressed in CIC-1 / by David St.John Astill. [Internet] [Thesis]. University of Adelaide; 1996. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2440/18707.

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

Council of Science Editors:

Astill DSJ. Characteristics of baculovirus - expressed in CIC-1 / by David St.John Astill. [Thesis]. University of Adelaide; 1996. Available from: http://hdl.handle.net/2440/18707

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

Indian Institute of Science

20. Harinath, S. Pharmacological Modulation Of Recombinant Human Two-Pore Domain K+ Channels : Whole-Cell patch-Clamp Analysis.

Degree: PhD, Faculty of Science, 2011, Indian Institute of Science

URL: http://etd.iisc.ac.in/handle/2005/1501

► Background potassium currents play an important role in the regulation of the resting membrane potential and excitability of mammalian neurons. Recently cloned two- pore domain… (more)

▼ Background potassium currents play an important role in the regulation of the resting membrane potential and excitability of mammalian neurons. Recently cloned two- pore domain potassium channels (K2p) are believed to underlie these currents. The roles of K2P channels in general anesthesia and neuroprotection have been proposed recently. In view of this, we investigated the ability of trichloroethanol (an active metabolite of the non-volatile general anesthetic cldoral hydrate, widely used as a pediatric sedative) to modulate the activity of human TREK-1 and TRAAK channels. We found that trichloroethanol potently activates both hTREK-1 and hTRAAK channels at pharmacologically relevant concentrations. The parent compound chloral hydrate was also found to augtnent the activity of both the channels reversibly. Studies with carboxy- terminal deletion mutants (hTREK-1A89, hTREK-1 A100 and hTREK-1 A1 19), suggested that C-terminal tail is not essential for the activation of TREK-1 by trichloroethanol. Our findings identify TREK-1 and TRCL4K channels as molecular targets for trichloroethanol and we propose that activation of both these channels might contribute to the CNS depressant effects of chloral hydrate. Another channel TASK-2, which is essentially absent in the human brain was also found to be potently activated by both trichloroethanol and chloral hydrate. In another series of experiments, we studied the effects of methyl xanthines caffeine and theophylline on hTREK-1 channels. Caffeine and theophylline are used for therapeutic purposes and frequently cause life-threatening convulsive seizures due to systemic toxicity. The mechanisms for the epileptogenicity of caffeine and theophylline are not clear. Recent experiments using knockout mice provided direct evidence for a role for TREK-1 in the control of epileptogenesis. We hypothesized that the epileptogenicity of caffeine and theophylline may be related to the inhibition of TREK-1 channels. We investigated this possibility and observed massive inhibition of TREK-1 channels at toxicologically relevant concentrations. Experiments with the mutant TREK-1 channel (S348A mutant) suggested the involvement of cANP/PKA pathway in the inhibition of TREK-1 channels by caffeine and theophylline. We suggest that inhibition of TREK-1 channels may contribute to the convulsive seizures induced by toxic levels of caffeine and theophylline. Local anesthetics exhibit their clinical effects not only by binding to voltage-gated sodium channels, but also by interacting with other ion channels such as potassium channels. Because of the physiological significance of TREK-1 channels and their abundant expression in peripheral sensory neurons, we investigated the effects of lidocaine to see whether its interaction with 'REK-1 channels contribute to the conduction blockade. Lidocaine caused dose-dependent inhibition of TREK-1channels and the inhibition was voltage-independent. Cytoplasmic C-terminal tail is critically required for lidocaine action. Inhibition of TREK-1 channels is… Advisors/Committee Members: Sikdar, S K (advisor).

Subjects/Keywords: K Channels - Physiology; K Channels - Pharmacology; Cell Patch-Clamp Analysis; Ion Channels; Two-Pore Domain Potassium Channels; K+ Channels; TREK-1 Channels; TRAAK Channels; Caffeine; Theophylline; K2P Channels; Molecular Biology

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

APA (6^th Edition):

Harinath, S. (2011). Pharmacological Modulation Of Recombinant Human Two-Pore Domain K+ Channels : Whole-Cell patch-Clamp Analysis. (Doctoral Dissertation). Indian Institute of Science. Retrieved from http://etd.iisc.ac.in/handle/2005/1501

Chicago Manual of Style (16^th Edition):

Harinath, S. “Pharmacological Modulation Of Recombinant Human Two-Pore Domain K+ Channels : Whole-Cell patch-Clamp Analysis.” 2011. Doctoral Dissertation, Indian Institute of Science. Accessed March 07, 2021. http://etd.iisc.ac.in/handle/2005/1501.

MLA Handbook (7^th Edition):

Harinath, S. “Pharmacological Modulation Of Recombinant Human Two-Pore Domain K+ Channels : Whole-Cell patch-Clamp Analysis.” 2011. Web. 07 Mar 2021.

Vancouver:

Harinath S. Pharmacological Modulation Of Recombinant Human Two-Pore Domain K+ Channels : Whole-Cell patch-Clamp Analysis. [Internet] [Doctoral dissertation]. Indian Institute of Science; 2011. [cited 2021 Mar 07]. Available from: http://etd.iisc.ac.in/handle/2005/1501.

Council of Science Editors:

Harinath S. Pharmacological Modulation Of Recombinant Human Two-Pore Domain K+ Channels : Whole-Cell patch-Clamp Analysis. [Doctoral Dissertation]. Indian Institute of Science; 2011. Available from: http://etd.iisc.ac.in/handle/2005/1501

Virginia Commonwealth University

21. Deng, Wu. ROLE OF ENDOTHELIN-1 IN THE REGULATION OF THE SWELLING-ACTIVATED Cl- CURRENT IN ATRIAL MYOCYTES.

Degree: PhD, Physiology, 2009, Virginia Commonwealth University

URL: https://doi.org/10.25772/Q669-NV98 ; https://scholarscompass.vcu.edu/etd/12

► Swelling-activated Cl- current (ICl,swell) is an outwardly rectifying Cl- current that influences cardiac electric activities and acts as a potential effector of mechanoelectrical feedback that… (more)

▼ Swelling-activated Cl- current (ICl,swell) is an outwardly rectifying Cl- current that influences cardiac electric activities and acts as a potential effector of mechanoelectrical feedback that antagonizes the effects of stretch-activated cation channels. Persistent activation of ICl,swell has been observed in multiple models of cardiovascular diseases. Previously we showed that angiotensin II (AngII) signaling and reactive oxygen species (ROS) produced by NADPH oxidase (NOX) are involved in the activation of ICl, swell by both beta1-integrin stretch and osmotic swelling. Because endothelin-1 (ET-1) is a potential downstream mediator of AngII and ETA receptor blockade abrogates AngII-induced ROS generation, we studied how ET-1 signaling regulates ICl,swell and the relationship between AngII and ET-1 signaling. Under isosmotic conditions, ET-1 elicited an outwardly rectifying Cl- current that was fully blocked by the highly selective ICl,swell inhibitor DCPIB and by osmotic shrinkage. Selective ETA blockade (BQ123), but not ETB blockade (BQ788), fully suppressed the ET-1-induced current. ET-1-induced ICl,swell was abolished by blockade of EGFR kinase (AG1478) and PI-3K inhibitors (LY294002 and wortmannin), which also suppress beta1-integrin stretch- and swelling-induced ICl,swell. ET-1-induced ICl,swell was abrogated by ebselen, a membrane-permeant glutathione peroxidase mimetic that dismutates H2O2 to H2O, suggesting that ROS were required intermediates in ET-1-induced activation of ICl,swell. Both NOX and mitochondria are important sources of ROS in cardiomyocytes. Blocking NOX with apocynin or mitochondrial complex I with rotenone both completely suppressed ET-1-induced ROS generation and activation of ICl,swell, indicating that ROS from both NOX and mitochondria were required to activate ICl,swell, and complete block by inhibitors of either ROS source suggests mitochondrial and NOX must act in series rather than in parallel. ICl,swell elicited by antimycin A, which stimulates superoxide production by mitochondrial complex III, was insensitive to NOX inhibitor apocynin and the NOX fusion peptide inhibitor gp91ds-tat. Activation of ICl,swell induced by diazoxide, which stimulates mitochondrial ROS production by opening mitochondrial KATP channels, was not affected by gp91ds-tat. These data suggests that mitochondrial ROS is downstream from NOX in the regulation of ICl,swell. Mitochondrial ROS production that is enhanced by NOX ROS is likely to be responsible for the activation of ICl,swell by ET-1. In order to determine the role of ERK in the proposed signaling pathway that regulates ICl,swell, we examined the effect of ERK inhibitors (PD 98059 and U0216) on the activation of ICl,swell elicited by ET-1, EGF, and H2O2. ERK inhibitors partially blocked ET-1-induced ICl,swell but fully inhibited activation of ICl,swell in response to EGF. However, ERK inhibitors did not affect ICl,swell elicited by exogenous H2O2. We also established the the relationship of ET-1 to AngII and osmotic swelling in the… Advisors/Committee Members: Clive Baumgarten.

Subjects/Keywords: ion channels; endothelin; reactive oxygen species; NADPH oxidase; mitochondria; cardiac myocytes; osmotic swelling; chloride channels; atrial myocytes; HL-1 cells; Life Sciences; Physiology

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

APA (6^th Edition):

Deng, W. (2009). ROLE OF ENDOTHELIN-1 IN THE REGULATION OF THE SWELLING-ACTIVATED Cl- CURRENT IN ATRIAL MYOCYTES. (Doctoral Dissertation). Virginia Commonwealth University. Retrieved from https://doi.org/10.25772/Q669-NV98 ; https://scholarscompass.vcu.edu/etd/12

Chicago Manual of Style (16^th Edition):

Deng, Wu. “ROLE OF ENDOTHELIN-1 IN THE REGULATION OF THE SWELLING-ACTIVATED Cl- CURRENT IN ATRIAL MYOCYTES.” 2009. Doctoral Dissertation, Virginia Commonwealth University. Accessed March 07, 2021. https://doi.org/10.25772/Q669-NV98 ; https://scholarscompass.vcu.edu/etd/12.

MLA Handbook (7^th Edition):

Deng, Wu. “ROLE OF ENDOTHELIN-1 IN THE REGULATION OF THE SWELLING-ACTIVATED Cl- CURRENT IN ATRIAL MYOCYTES.” 2009. Web. 07 Mar 2021.

Vancouver:

Deng W. ROLE OF ENDOTHELIN-1 IN THE REGULATION OF THE SWELLING-ACTIVATED Cl- CURRENT IN ATRIAL MYOCYTES. [Internet] [Doctoral dissertation]. Virginia Commonwealth University; 2009. [cited 2021 Mar 07]. Available from: https://doi.org/10.25772/Q669-NV98 ; https://scholarscompass.vcu.edu/etd/12.

Council of Science Editors:

Deng W. ROLE OF ENDOTHELIN-1 IN THE REGULATION OF THE SWELLING-ACTIVATED Cl- CURRENT IN ATRIAL MYOCYTES. [Doctoral Dissertation]. Virginia Commonwealth University; 2009. Available from: https://doi.org/10.25772/Q669-NV98 ; https://scholarscompass.vcu.edu/etd/12

Universitat de Barcelona

22. Pérez Rius, Carla. Model animal de malalties associades a canals de clorur en peix zebra.

Degree: Departament de Ciències Fisiològiques, 2017, Universitat de Barcelona

URL: http://hdl.handle.net/10803/482037

► Chloride is the most abundant anion in body fluids. Chloride transport is involved in many different cellular processes, such as regulating the excitability of muscle… (more)

▼ Chloride is the most abundant anion in body fluids. Chloride transport is involved in many different cellular processes, such as regulating the excitability of muscle cells, transepithelial transport and regulation of pH in lysosomes, among others. The ClC protein family comprises a group of proteins allowing this exchange between the intracellular and extracellular space. They are divided into two subgroups: the plasma membrane chloride channels and the Cl-/H+ co-transporters located in intracellular compartments. The plasma membrane chloride channels are ClC-1 (muscle-specific, is in charge of keeping the resting membrane potential in muscle cells), ClC-2 (ubiquitously expressed) and ClC-Ka and ClC-Kb (located in the distal renal tubule and inner ear, involved in renal salt reabsorption and sound transduction in the ear). Mutations in the genes encoding for these channels lead to human rare diseases. Loss of ClC-1 leads to Myotonia congenital resulting in hyperexcitable muscles, lack of ClC-2 leads to a rare type of vacuolating leukodystrophy and the loss of ClC-Kb leads to Bartter syndrome type III, which is characterized by renal salt loss. In this thesis, we have identified and characterized the zebrafish (Danio rerio) ClC orthologs. To accomplish that, we have generated and validated antibodies against the zebrafish proteins. Furthermore, we have developed transgenesis tools for native and mutant proteins expression experiments and generated clcn1a and clcn1b (human CLCN1 orthologs) loss-of-function alleles in zebrafish with CRISPR/Cas9 technology (the clcn1 null-mutant is in progress). We have validated these lines as knock out and a preliminary locomotor characterization shows these animals display normal spontaneous movement and no difference has been observed between wild-type and knock out animals when applying vibrational stimulus. We hope for the clcn1a-/- clcn1b-/- to show locomotor deficiencies reminiscent to those observed in Myotonia congenita patients. Advisors/Committee Members: [email protected] (authoremail), false (authoremailshow), Estévez Povedano, Raúl (director), Barrallo-Gimeno, Alejandro (director), Estévez Povedano, Raúl (tutor), true (authorsendemail).

Subjects/Keywords: Fisiologia; Fisiología; Physiology; Aparell locomotor; Aparato locomotor; Musculoskeletal system; Canals de clorur; Canales de cloruros; Chloride channels; Peix zebra; Pez cebra; Zebra danio; Proteïnes; Proteínas; Proteins; Ciències de la Salut; 612

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

APA (6^th Edition):

Pérez Rius, C. (2017). Model animal de malalties associades a canals de clorur en peix zebra. (Thesis). Universitat de Barcelona. Retrieved from http://hdl.handle.net/10803/482037

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):

Pérez Rius, Carla. “Model animal de malalties associades a canals de clorur en peix zebra.” 2017. Thesis, Universitat de Barcelona. Accessed March 07, 2021. http://hdl.handle.net/10803/482037.

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

MLA Handbook (7^th Edition):

Pérez Rius, Carla. “Model animal de malalties associades a canals de clorur en peix zebra.” 2017. Web. 07 Mar 2021.

Vancouver:

Pérez Rius C. Model animal de malalties associades a canals de clorur en peix zebra. [Internet] [Thesis]. Universitat de Barcelona; 2017. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/10803/482037.

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

Council of Science Editors:

Pérez Rius C. Model animal de malalties associades a canals de clorur en peix zebra. [Thesis]. Universitat de Barcelona; 2017. Available from: http://hdl.handle.net/10803/482037

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

23. Dobbins, George C. (George Clement). The role of the cytoskeleton in AChR clustering.

Degree: PhD, 2007, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,119

►

The human brain contains billions of neurons which are designed to receive and integrate a range of electrical and biochemical signals. The ability to convey… (more)

▼

The human brain contains billions of neurons which are designed to receive and integrate a range of electrical and biochemical signals. The ability to convey information between these cells depends on synapses. A precise apposition between the pre and post synapse must exist for efficient transmission to occur. The neuromuscular junction (NMJ) has become a model for studying synaptogenesis. Although much is known about the steps in NMJ formation, only recently have there been insights into the mechanism behind NMJ development. Much of this research has focused on how acetylcholine receptors (AChRs) at the postsynapse form clusters directly apposed to the presynapse. One protein that is required for AChR clustering is rapsyn. Rapsyn is thought to anchor the AChR to the cytoskeleton; however, little is known about the mechanism behind rapsyn’s interaction with the cytoskeleton. In order to further elucidate rapsyn’s role, we performed a yeast two-hybrid screen with rapsyn as the bait. One protein we found was [alpha]-actinin, a cytoskeletal protein that crosslinks actin. Through further yeast two-hybrid studies, we mapped which domains with in [alpha]-actinin and rapsyn were responsible for their interaction. Furthermore, we were able to show that [alpha]-actinin interacts directly with rapsyn. Experiments showed that the rapsyn-[alpha]-actinin interaction was weak in both heterologous cells and in myotubes. However, the rapsyn-[alpha]-actinin interaction was found to be increased by factors known to stimulate AChR clustering. Similarly, agrin, the most studied AChR clustering agent, increased the AChR’s interaction with [alpha]-actinin in a manner dependent on rapsyn. Also, we found that knocking down [alpha]-actinin expression via an [alpha]-actinin specific miRNAi construct disrupted AChR clustering. Furthermore, inhibition of Abl, a tyrosine kinase required for AChR clustering, disrupted the agrin regulated rapsyn-[alpha]-actinin interaction. Finally, and perhaps most interesting, an ACh agonist known to disperse AChR clusters abolished the rapsyn-[alpha]-actinin interaction. Together these results indicate a potentially important role for [alpha]-actinin in AChR clustering.

Ph.D

ix, 92 p. : ill., digital, PDF file.

Neurobiology

Joint Health Sciences

Neuromuscular junction Rapsyn Alpha-actinin Acetylcholine receptor Cytoskeleton Synapse

UNRESTRICTED

Advisors/Committee Members: Mei, Lin, Theibert, Anne , Keyser, Kent , Wilson, Scott , Woods, Anne.

Subjects/Keywords: Cytoskeleton – physiology <; br>; Neuromuscular Junction – physiology <; br>; Receptors, Cholinergic – physiology

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

APA (6^th Edition):

Dobbins, G. C. (. C. (2007). The role of the cytoskeleton in AChR clustering. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,119

Chicago Manual of Style (16^th Edition):

Dobbins, George C (George Clement). “The role of the cytoskeleton in AChR clustering.” 2007. Doctoral Dissertation, University of Alabama – Birmingham. Accessed March 07, 2021. http://contentdm.mhsl.uab.edu/u?/etd,119.

MLA Handbook (7^th Edition):

Dobbins, George C (George Clement). “The role of the cytoskeleton in AChR clustering.” 2007. Web. 07 Mar 2021.

Vancouver:

Dobbins GC(C. The role of the cytoskeleton in AChR clustering. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2007. [cited 2021 Mar 07]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,119.

Council of Science Editors:

Dobbins GC(C. The role of the cytoskeleton in AChR clustering. [Doctoral Dissertation]. University of Alabama – Birmingham; 2007. Available from: http://contentdm.mhsl.uab.edu/u?/etd,119

University of Missouri – Columbia

24. Lett, Kawasi M. Loss of afferent input alters voltage gated ion channel and neuromodulator receptor expression in crustacean and mammalian neurons.

Degree: 2014, University of Missouri – Columbia

URL: http://hdl.handle.net/10355/45807

► [ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] Neural networks need to generate appropriate output regardless of external stimuli, to ensure survival of… (more)

Subjects/Keywords: Neurotransmitter receptors; Neurons – Physiology; Homeostasis; Ion channels

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

APA (6^th Edition):

Lett, K. M. (2014). Loss of afferent input alters voltage gated ion channel and neuromodulator receptor expression in crustacean and mammalian neurons. (Thesis). University of Missouri – Columbia. Retrieved from http://hdl.handle.net/10355/45807

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):

Lett, Kawasi M. “Loss of afferent input alters voltage gated ion channel and neuromodulator receptor expression in crustacean and mammalian neurons.” 2014. Thesis, University of Missouri – Columbia. Accessed March 07, 2021. http://hdl.handle.net/10355/45807.

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

MLA Handbook (7^th Edition):

Lett, Kawasi M. “Loss of afferent input alters voltage gated ion channel and neuromodulator receptor expression in crustacean and mammalian neurons.” 2014. Web. 07 Mar 2021.

Vancouver:

Lett KM. Loss of afferent input alters voltage gated ion channel and neuromodulator receptor expression in crustacean and mammalian neurons. [Internet] [Thesis]. University of Missouri – Columbia; 2014. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/10355/45807.

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

Council of Science Editors:

Lett KM. Loss of afferent input alters voltage gated ion channel and neuromodulator receptor expression in crustacean and mammalian neurons. [Thesis]. University of Missouri – Columbia; 2014. Available from: http://hdl.handle.net/10355/45807

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

25. Davison, Ryan C. The behavior of oculomotor neurons during conjugate and disconjugate eye movements.

Degree: PhD, 2007, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,435

►

Conjugate eye movements are those that occur when both eyes move the same amount in the same direction. Saccades and smooth pursuit have classically been… (more)

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Conjugate eye movements are those that occur when both eyes move the same amount in the same direction. Saccades and smooth pursuit have classically been considered conjugate movements, however to view objects of different distances requires disconjugate, vergence eye movements. When gaze is transferred in a three-dimensional environment, saccadic and vergence eye movements are often combined, resulting in disjunctive eye movements characterized by unequal movements of the two eyes. A consequence of such disjunctive eye movements is a significant intrasaccadic enhancement in the normally slow velocities observed during vergence. It has been proposed that such disjunctive eye movements are generated either binocularly through a combination of separate saccadic and vergence subsystems (Hering) and an enhanced vergence velocity signal, or monocularly through independent left and right eye subsystems (Helmholtz) and unequal saccadic commands to the two eyes. To investigate the underlying mechanisms of disjunctive eye movements during combined saccade-vergence eye movements, we recorded from medial rectus motoneurons (MRMNs) in alert, behaving Rhesus monkeys (Macaca mulatta). Medial rectus motoneurons were studied because they represent a final common output pathway where all relevant oculomotor signals are present. Single-unit recording was conducted from 72 MRMNs in three animals. Data were collected as animals engaged in a variety of saccadic, vergence, and smooth pursuit eye movements, and the relationships between neuronal firing patterns and eye position and velocity were analyzed. First, we characterized the position and velocity signals present on MRMNs during smooth pursuit, saccades, and vergence eye movements. Second, in the same population, we characterized the signals present during combined saccade-vergence eye movements that resulted in significant intrasaccadic vergence velocity enhancements. It was found that individual MRMN behavior varied significantly depending on the type of eye movement that was executed. As a result, individual MRMNs exhibited significantly different static and dynamic sensitivities for smooth pursuit, saccades, and vergence eye movements. We also found that the activity of a MRMN during combined saccade-vergence eye movements was better correlated with the activity of that neuron during smooth symmetric vergence than during conjugate saccadic eye movements. This suggests that the neural signal underlying enhanced vergence velocities during combined saccade-vergence eye movements arises from the vergence eye movement subsystem.

x, 95 p. : ill., digital, PDF file

Psychology

Social and Behavioral Sciences

Oculomotor Medial Rectus Motoneurons

UNRESTRICTED

Advisors/Committee Members: Gamlin, Paul, Amthor, Frank Busettini, Claudio Cox, James Weller, Rosalyn.

Subjects/Keywords: Convergence, Ocular – physiology<; br>; Eye Movements – physiology<; br>; Motor Neurons – physiology<; br>; Pursuit, Smooth – physiology<; br>; Saccades – physiology

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

APA (6^th Edition):

Davison, R. C. (2007). The behavior of oculomotor neurons during conjugate and disconjugate eye movements. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,435

Chicago Manual of Style (16^th Edition):

Davison, Ryan C. “The behavior of oculomotor neurons during conjugate and disconjugate eye movements.” 2007. Doctoral Dissertation, University of Alabama – Birmingham. Accessed March 07, 2021. http://contentdm.mhsl.uab.edu/u?/etd,435.

MLA Handbook (7^th Edition):

Davison, Ryan C. “The behavior of oculomotor neurons during conjugate and disconjugate eye movements.” 2007. Web. 07 Mar 2021.

Vancouver:

Davison RC. The behavior of oculomotor neurons during conjugate and disconjugate eye movements. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2007. [cited 2021 Mar 07]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,435.

Council of Science Editors:

Davison RC. The behavior of oculomotor neurons during conjugate and disconjugate eye movements. [Doctoral Dissertation]. University of Alabama – Birmingham; 2007. Available from: http://contentdm.mhsl.uab.edu/u?/etd,435

26. Cottingham, Christopher. Neuropharmacology Of The α2a Adrenergic Receptor In Disorders Of Mood And Cognition.

Degree: PhD, 2012, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,1393

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Depressive disorders carry relatively high lifetime risks of greater than 10%, and the antidepressant drugs used in the pharmacotherapy of these mood/cognitive disorders are among… (more)

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Depressive disorders carry relatively high lifetime risks of greater than 10%, and the antidepressant drugs used in the pharmacotherapy of these mood/cognitive disorders are among the most-prescribed pharmacological agents. However, a detailed understanding of both depressive etiology and the pharmacological mechanisms of action for antidepressant drugs remain elusive. The overall goal of this dissertation research is to provide novel in-sights through a detailed study of the neuropharmacology of the α2A<</drenergic receptor (AR). α2<</s, as key regulators of noradrenergic neurotransmission, have been broadly understood to have some ill-defined role in both the neurobiology and neuropharmacology of depressive disorders. The studies contained within this dissertation have been aimed at investigating the role of the α2A<</ in antidepressant neuropharmacology, focusing on the tricyclic antidepressant drug desipramine (DMI) as a model compound. I have studied the actions of DMI at the α2A<</ on several levels. First, I have demonstrated that the in vivo<</> antidepressant behavioral effects of DMI in the rodent forced swim test model are dependent on α2A<</s (Cottingham et al., 2012, Neuropharmacology<</>, doi:10.1016/j.neuropharm.2012.02.011). Further, this study has indicated that DMI achieves these antidepressant effects through direct engagement of the α2A<</ and arrestin, with reciprocal regulation by the dendritic protein spinophilin. Secondly, I have characterized the pharmacological and functional properties of the interaction of DMI with the α2A<</ (Cottingham et al., J. Biol. Chem.<</> 286<</ 36063-75), finding DMI to be the first example of an arrestin-biased ligand at the α2A<</. This interaction does not drive receptor signaling, but rather arrestin-dependent downregulation of central receptors with chronic DMI exposure in vitro<</> and in vivo<</>. These data provide extremely novel insight into previously unexplained neuroadaptive changes in receptor expression associated with antidepressant drugs. Finally, my findings on modulation of endogenous agonist-induced α2A<</ signaling by DMI provide evidence that has implications for both the depressive role of α2A<</s and the molecular pharmacology of these physiologically important receptors (Cottingham et al., BBRC<</>, doi:10.1016/j.bbrc.02.2012.135). Overall, my findings have validated the importance of the α2A<</ in depressive disorders, and identified direct biased targeting of the receptor and its interacting regulators as a novel therapeutic antidepressant strategy.

PhD

1 online resource (xii, 140 p.) :ill., digital, PDF file.

Joint Health Sciences

alpha2 adrenergic receptor antidepressant arrestin downregulation forced swim test spinophilin

UNRESTRICTED

Advisors/Committee Members: Qin Wang, Bevensee, Mark O. Li,Xiaohua McMahon, Lori L. Wyss,J Michael.

Subjects/Keywords: Actins – metabolism<; br>; Amygdala – physiology<; br>; Conditioning, Classical – physiology.<; br>; Fear – physiology<; br>; Long-Term Potentiation – physiology.<; br>; Memory – physiology<; br>; Nonmuscle Myosin Type IIB – metabolism.<; br>; Synapses – physiology

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

APA (6^th Edition):

Cottingham, C. (2012). Neuropharmacology Of The α2a Adrenergic Receptor In Disorders Of Mood And Cognition. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1393

Chicago Manual of Style (16^th Edition):

Cottingham, Christopher. “Neuropharmacology Of The α2a Adrenergic Receptor In Disorders Of Mood And Cognition.” 2012. Doctoral Dissertation, University of Alabama – Birmingham. Accessed March 07, 2021. http://contentdm.mhsl.uab.edu/u?/etd,1393.

MLA Handbook (7^th Edition):

Cottingham, Christopher. “Neuropharmacology Of The α2a Adrenergic Receptor In Disorders Of Mood And Cognition.” 2012. Web. 07 Mar 2021.

Vancouver:

Cottingham C. Neuropharmacology Of The α2a Adrenergic Receptor In Disorders Of Mood And Cognition. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2012. [cited 2021 Mar 07]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1393.

Council of Science Editors:

Cottingham C. Neuropharmacology Of The α2a Adrenergic Receptor In Disorders Of Mood And Cognition. [Doctoral Dissertation]. University of Alabama – Birmingham; 2012. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1393

27. Olteanu, Dragos S. Dysregulated ENAC and NHE function in cilium-deficient renal collecting duct cell monolayers : a model of polycystic kidney disease.

Degree: PhD, 2007, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,610

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Polycystic kidney disease in both its recessive and dominant forms involves the remodeling of the kidney and extra-renal tissues where parts of the tissue break… (more)

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Polycystic kidney disease in both its recessive and dominant forms involves the remodeling of the kidney and extra-renal tissues where parts of the tissue break contact with the normal tissue as “pseudocysts” or fully encapsulated and fluid-filled cysts. Once this remodeling into “cystic” tissue has occurred, the secondary progression of the disease is influenced dramatically by salt and water transport and by autocrine and paracrine factors that become trapped in these abnormal cystic microenvironments. During this progression, hypertension develops ahead of renal decline. In recessive PKD (ARPKD), there is early onset hypertension in neonatal and pediatric patients that is severe and debilitating. My research has focused on cilium-deficient cortical collecting duct principal cell models of PKD from the Tg737orpk mouse. My work is being extended to conditional cilium-deficient cell models as well as the mouse models from which these cells were derived. I have found that ENaC is 4-fold upregulated in cilium-deficient versus cilium-competent cell monolayers. This upregulation may be central to the rapid development of hypertension. In parallel, there is inappropriate mislocalization of sodium/hydrogen (Na/H) exchange (NHE) in the apical membrane of cilium-deficient cell monolayers versus controls. Together, apical NHE activity with ENaC upregulation may contribute marked Na+ hyperabsorption leading to hypertension in ARPKD and, perhaps, ADPKD patients. This cilium-deficient pathology creates an intriguing pathophysiology where NHEs and ENaC are in the same apical membrane domain in principal cells. Apical NHE activity would fuel ENaC activity via extracellular acidification and intracellular alkalinization. Metabolic pH measurements of freshly voided urine showed enhanced acidification in the mutant mice at all ages between 1 and 4 weeks. Metabolic alkalosis developed at 4 weeks of age. My future work will seek to understand why the loss of a sensory organelle, the primary or central monocilium, leads to upregulation of salt and water reabsorption in terms of epithelial cell pathophysiology. Steps designed to quell salt hyperabsorption may be beneficial in controlling the establishment and progression of cystic kidney disease in humans.

1 online resource (xii, 227 p. : ill., digital, PDF file)

Physiology and Biophysics

Joint Health Sciences;

kidney cell physiology sodium transport polycystic kidney disease epithelial cell acid-base transport

UNRESTRICTED

Advisors/Committee Members: Schwiebert, Erik M., Bevensee, Mark O. , Clancy, John P. , Smith, Peter R. , Yoder, Bradley K..

Subjects/Keywords: Cilia – metabolism<; br>; Epithelial Cells<; br>; Kidney<; br>; Polycystic Kidney, Autosomal Recessive – metabolism<; br>; Sodium – metabolism<; br>; Sodium Channels – metabolism

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

APA (6^th Edition):

Olteanu, D. S. (2007). Dysregulated ENAC and NHE function in cilium-deficient renal collecting duct cell monolayers : a model of polycystic kidney disease. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,610

Chicago Manual of Style (16^th Edition):

Olteanu, Dragos S. “Dysregulated ENAC and NHE function in cilium-deficient renal collecting duct cell monolayers : a model of polycystic kidney disease.” 2007. Doctoral Dissertation, University of Alabama – Birmingham. Accessed March 07, 2021. http://contentdm.mhsl.uab.edu/u?/etd,610.

MLA Handbook (7^th Edition):

Olteanu, Dragos S. “Dysregulated ENAC and NHE function in cilium-deficient renal collecting duct cell monolayers : a model of polycystic kidney disease.” 2007. Web. 07 Mar 2021.

Vancouver:

Olteanu DS. Dysregulated ENAC and NHE function in cilium-deficient renal collecting duct cell monolayers : a model of polycystic kidney disease. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2007. [cited 2021 Mar 07]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,610.

Council of Science Editors:

Olteanu DS. Dysregulated ENAC and NHE function in cilium-deficient renal collecting duct cell monolayers : a model of polycystic kidney disease. [Doctoral Dissertation]. University of Alabama – Birmingham; 2007. Available from: http://contentdm.mhsl.uab.edu/u?/etd,610

University of New South Wales

28. Warton, Kristina. Characterization of CLIC1 : a chloride ion channel which can exist in both a transmembrane and a soluble state.

Degree: Medicine. Clinical School - St Vincent's Hospital, 2002, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/64448 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:62158/SOURCE01?view=true

Subjects/Keywords: Chloride channels; Ion channels; Cell membranes; Thesis Digitisation Program

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

APA (6^th Edition):

Warton, K. (2002). Characterization of CLIC1 : a chloride ion channel which can exist in both a transmembrane and a soluble state. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/64448 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:62158/SOURCE01?view=true

Chicago Manual of Style (16^th Edition):

Warton, Kristina. “Characterization of CLIC1 : a chloride ion channel which can exist in both a transmembrane and a soluble state.” 2002. Doctoral Dissertation, University of New South Wales. Accessed March 07, 2021. http://handle.unsw.edu.au/1959.4/64448 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:62158/SOURCE01?view=true.

MLA Handbook (7^th Edition):

Warton, Kristina. “Characterization of CLIC1 : a chloride ion channel which can exist in both a transmembrane and a soluble state.” 2002. Web. 07 Mar 2021.

Vancouver:

Warton K. Characterization of CLIC1 : a chloride ion channel which can exist in both a transmembrane and a soluble state. [Internet] [Doctoral dissertation]. University of New South Wales; 2002. [cited 2021 Mar 07]. Available from: http://handle.unsw.edu.au/1959.4/64448 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:62158/SOURCE01?view=true.

Council of Science Editors:

Warton K. Characterization of CLIC1 : a chloride ion channel which can exist in both a transmembrane and a soluble state. [Doctoral Dissertation]. University of New South Wales; 2002. Available from: http://handle.unsw.edu.au/1959.4/64448 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:62158/SOURCE01?view=true

29. Rubio, Maria Dolores. Myosin II in hippocampal synapses: regulation of synaptic plasticity, strength and actin dynamics by two distinct isoforms.

Degree: PhD, 2011, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,878

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Cytoskeletal actin filaments underlie dendritic spine plasticity, critical for several forms of learning and memory. Therefore, understanding the mechanisms that regulate actin dynamics is essential… (more)

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Cytoskeletal actin filaments underlie dendritic spine plasticity, critical for several forms of learning and memory. Therefore, understanding the mechanisms that regulate actin dynamics is essential to elucidate memory formation pathways. Myosins, a superfamily of actin binding proteins, have emerged as candidates for regulation of actin dynamics in the brain. Several myosin class II isoforms have been identified in brain, but their individual contribution to synaptic activity is still unknown. Based on the finding that myosin IIB regulates actin polymerization in the growth cone of developing neurons and that it is necessary for maintenance of dendritic spine structure, I hypothesized that in dendritic spines myosin IIB regulates actin dynamics, affecting synaptic transmission. I show that in addition to basal transmission, myosin IIB affects the maintenance of long term potentiation through a mechanism leading to reorganization and de novo synthesis of actin filaments. I further show that myosin IIB activity on actin filaments is critical for long-term memory consolidation. In addition to advancing our understanding of myosin IIB function in neurons, I was also able to characterize and identify a distinct muscle isoform of myosin II, MyH7B, in brain. The effects on dendritic spine morphology and synaptic strength of this isoform are different from those of myosin IIB. MyH7B acts as a structural myosin that maintains synaptic morphology and regulates trafficking of AMPA receptors to the synaptic surface through its activity on actin filament dynamics. Through my research I was able to identify a novel function for two distinct myosin II isoforms in brain, finding them critical for synaptic activity.

1 online resource (viii, 205 p. : ill., digital, PDF file)

Neurobiology;

Joint Health Sciences;

actin myosin dendritic spine synaptic transmission AMPA receptors plasticity

UNRESTRICTED

Advisors/Committee Members: Rumbaugh, Gavin, McMahon, Lori L. , Sontheimer, Harald , Sweatt, J. David , Wilson, Scott.

Subjects/Keywords: Actins – metabolism<; br>; Cardiac Myosins – physiology<; br>; Long-Term Potentiation – physiology<; br>; Memory – physiology<; br>; Myosin Heavy Chains – physiology<; br>; Neurons – metabolism<; br>; Nonmuscle Myosin Type IIB – metabolism<; br>; Synapses – physiology

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

APA (6^th Edition):

Rubio, M. D. (2011). Myosin II in hippocampal synapses: regulation of synaptic plasticity, strength and actin dynamics by two distinct isoforms. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,878

Chicago Manual of Style (16^th Edition):

Rubio, Maria Dolores. “Myosin II in hippocampal synapses: regulation of synaptic plasticity, strength and actin dynamics by two distinct isoforms.” 2011. Doctoral Dissertation, University of Alabama – Birmingham. Accessed March 07, 2021. http://contentdm.mhsl.uab.edu/u?/etd,878.

MLA Handbook (7^th Edition):

Rubio, Maria Dolores. “Myosin II in hippocampal synapses: regulation of synaptic plasticity, strength and actin dynamics by two distinct isoforms.” 2011. Web. 07 Mar 2021.

Vancouver:

Rubio MD. Myosin II in hippocampal synapses: regulation of synaptic plasticity, strength and actin dynamics by two distinct isoforms. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2011. [cited 2021 Mar 07]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,878.

Council of Science Editors:

Rubio MD. Myosin II in hippocampal synapses: regulation of synaptic plasticity, strength and actin dynamics by two distinct isoforms. [Doctoral Dissertation]. University of Alabama – Birmingham; 2011. Available from: http://contentdm.mhsl.uab.edu/u?/etd,878

University of Hong Kong

30. Li, Xiang. Using alpha-aminoxy acids as building blocks to construct anion receptors and synthetic chloride channels.

Degree: 2008, University of Hong Kong

URL: http://hdl.handle.net/10722/50389

Subjects/Keywords: Chloride channels.; Anions - Receptors.; Amino acids.

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

APA (6^th Edition):

Li, X. (2008). Using alpha-aminoxy acids as building blocks to construct anion receptors and synthetic chloride channels. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/50389

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):

Li, Xiang. “Using alpha-aminoxy acids as building blocks to construct anion receptors and synthetic chloride channels.” 2008. Thesis, University of Hong Kong. Accessed March 07, 2021. http://hdl.handle.net/10722/50389.

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

MLA Handbook (7^th Edition):

Li, Xiang. “Using alpha-aminoxy acids as building blocks to construct anion receptors and synthetic chloride channels.” 2008. Web. 07 Mar 2021.

Vancouver:

Li X. Using alpha-aminoxy acids as building blocks to construct anion receptors and synthetic chloride channels. [Internet] [Thesis]. University of Hong Kong; 2008. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/10722/50389.

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

Council of Science Editors:

Li X. Using alpha-aminoxy acids as building blocks to construct anion receptors and synthetic chloride channels. [Thesis]. University of Hong Kong; 2008. Available from: http://hdl.handle.net/10722/50389

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

Open Access Theses and Dissertations