Relevant bibliographies by topics / T-type calcium channel inhibitors

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Academic literature on the topic 'T-type calcium channel inhibitors'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

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Dissertations / Theses on the topic "T-type calcium channel inhibitors"

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Anhettigama, Gamaralalage Medha Jaimini Gunaratna. "Design, synthesis and bio-evaluation of piperidines and CGRP peptides; Synthesis of substituted 6-(dimethylamino)-2-phenylisoindolin-1-ones for the inhibition of luciferase." Diss., Kansas State University, 2017. http://hdl.handle.net/2097/38204.

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Doctor of Philosophy<br>Department of Chemistry<br>Duy H. Hua<br>Three research projects are described in this dissertation, and they are: (i) discovery of piperidine derivatives as T-type calcium channel inhibitors for the treatment of epilepsy and neuropathic pain and as protein disulfide isomerase inhibitors for the treatment of influenza viral infection; (ii) discovery of peptide-based calcitonin gene-related peptide receptor antagonists for the treatment of inflammatory pain; and (iii) synthesis of substituted 6-(dimethylamino)-2-phenylisoindolin-1-ones for the inhibition of luciferase.
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Francois, Amaury. "Distributions et fonctions du canal Calcique Cav3.2 dans les voies somatosensorielles." Thesis, Montpellier 2, 2013. http://www.theses.fr/2013MON20036/document.

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Le traitement et la gestion de la douleur sont depuis toujours une priorité pour le corps médical. Malgré leur importance pour la qualité de vie, les analgésiques couramment utilisés possèdent un ratio bénéfice/risque faible. La recherche de nouveaux concepts thérapeutiques pour lutter contre la douleur est donc une priorité. Afin de répondre à ce besoin, il faut d'abord comprendre les mécanismes de la perception de la douleur ainsi que, plus globalement, ceux permettant de percevoir son environnement. Dans ce contexte, de nombreuses études ont mis en évidence l'implication du canal calcique à
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Florczak, Kaya. "Wnt/β-Catenin Signalling Inhibits T-Type Calcium Channels in Cardiomyocytes". Thesis, Université d'Ottawa / University of Ottawa, 2021. http://hdl.handle.net/10393/41983.

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Background: The Wnt/β-catenin signalling pathway is activated in arrhythmogenic heart diseases such as myocardial infarction and heart failure, but it is unclear if the pathway regulates cardiac ion channels and thus may play a role in arrhythmogenesis. Previous PCR array screening from our lab showed that the transcript level of the T-type calcium channel gene Cacna1g was reduced in primary culture of neonatal rat ventricular myocytes (NRVMs) after activation of Wnt/β-catenin signalling with Wnt3a protein (100 ng/ml) or a small molecule activator of the pathway, CHIR (3 µM) (n=3, p<0.01). In
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NIWA, Noriko, Kenji YASUI, and Itsuo KODAMA. "Inhibitory Action of Mibefradil on T-Type Calcium Channels in Early Embryonic Mouse Ventricular Myocytes." Research Institute of Environmental Medicine, Nagoya University, 2002. http://hdl.handle.net/2237/2792.

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Wang, Fang. "DOES CALCIUM INFLUX THROUGH T-TYPE CALCIUM CHANNEL INDUCE CARDIOMYOCYTE PROLIFERATION?" Diss., Temple University Libraries, 2012. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/214814.

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Physiology<br>Ph.D.<br>Cardiovascular disease remains the number one cause or mortally in the western world. Heart failure is the most rapidly growing cardiovascular disease (Hobbs, 2004; Levy, et al., 2002). Heart failure, by definition, is progressive deteriorating function of the heart due to progressive cardiac myocytes loss. Though after decades of endeavor of searching the pathophysiology and treatments for heart failure, it remains highly lethal. Therefore, it is vital to find novel therapies to help treat such chronic disease. Replace the lost cardiomyocyte with new ones could restore
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Foster, Nicholas E. V. "Whole cell and single channel analysis of cloned T-type calcium channel functionally expressed in HEK cells." Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=29435.

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I examined the kinetic properties of macroscopic and single channel currents produced by an isoform of the rat CaV3.1 T-type voltage-gated calcium channel, expressed in HEK-293 cells. Whole cell currents were measured in 2 mM extracellular Ca2+, and single channel activity was recorded from cell-attached patches in 120 mM Ba2+. We found that macroscopic rates of activation, deactivation, inactivation, and recovery from inactivation each have voltage-dependent and voltage-independent components. Single channels opened and closed rapidly in bursts before inactivating, with a mean open time of 1
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Hildebrand, Michael Earl. "Differential modulation of T-type voltage gated calcium channels by G-protein coupled receptors." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/1019.

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T-type voltage-gated calcium (Ca2+) channels play critical roles in controlling neuronal excitability, firing patterns, and synaptic plasticity, although the mechanisms and extent to which T-type Ca2+ channels are modulated by G-protein coupled receptors (GPCRs) remains largely unexplored. Investigations into T-type modulation within native neuronal systems have been complicated by the presence of multiple GPCR subtypes and a lack of pharmacological tools to separate currents generated by the three T-type isoforms; Cav3.1, Cav3.2, and Cav3.3. We hypothesize that specific Cav3 subtypes play u
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8

Li, Yingxin. "THE ROLES OF Cav3.1/a1G T-TYPE CALCIUM CHANNEL IN HEART RATE GENERATION, REGULATION AND CARDIAC ARRHYTHMIAS." Diss., Temple University Libraries, 2011. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/151806.

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Physiology<br>Ph.D.<br>T-type Ca²+ channels (TTCCs) are expressed in cardiac pacemaker cells and conduction system of mammals. However, the roles of TTCCs in heart rate (HR) generation and regulation, and arrhythmias are not well understood. In the mouse, the major TTCC expressed in the heart is Cav3.1/a1G, and therefore we used Cav3.1/ 1G transgenic (TG) and knockout (KO) mice respectively to define the role of TTCC in the heart rate generation, regulation and arrhythmias. Telemetric (conscious) and surface (anesthetized) electrocardiogram (ECG) were used to determine the baseline HR and the
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Cunningham, Jonathan. "Differential effects of the t-type calcium channel antagonist, Z944, on behaviours associated with amphetamine and morphine addiction." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/59529.

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Mixed L-/T-type calcium channel antagonists attenuate morphine- and amphetamine induced conditioned place preference (CPP). Subtype specific antagonists for T-type calcium channels attenuate nicotine-reinforced behaviours in rats. This thesis investigated the effects of a novel T-type calcium channel antagonist, Z944, on the acquisition, expression, and reinstatement of amphetamine and morphine CPP. Furthermore, we examined Z944 for aversive or rewarding properties, and determined changes in locomotion with Z944 alone and in conjunction with amphetamine or morphine. CPP was induced with either
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Mulatz, Kirk James. "A PDZ-3 mediated physical and functional interaction between the CaV3.2 T-type calcium channel and neuronal nitric oxide synthase." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/43790.

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T-type voltage-gated calcium channels are expressed throughout the central and peripheral nervous systems as well as in several non-neuronal tissues and contribute to variety of functions such as neuronal excitability, intracellular calcium influx, shaping action potentials, pace-making activity, hormone secretion, and neurotransmitter release. Of the three T-type channel isoforms, Cav3.2 is uniquely sensitive to redox modulation with oxidizing reagents inhibiting and reducing compounds enhancing channel activity. This modulation has been shown to alter firing patterns of reticular thalamic ne
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